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1
Perić, Aleksandar, Danilo Vojvodić, Biserka Vukomanović-Đurđević, and Nenad Baletić. "Eosinophilic Inflammation in Allergic Rhinitis and Nasal Polyposis." Archives of Industrial Hygiene and Toxicology 62, no. 4 (2011): 341–48. http://dx.doi.org/10.2478/10004-1254-62-2011-2120.
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Eosinophilic Inflammation in Allergic Rhinitis and Nasal PolyposisOn histopathological examination, nasal polyps and nasal mucosa in allergic rhinitis show different forms of pseudostratified respiratory epithelium, whereas the dominant characteristic of lamina propria is an eosinophilic infiltration. The aim of this study was to compare interleukin (IL)-5 and eosinophilic cationic protein (ECP) levels in the nasal fluid of 42 patients: 12 with allergic rhinitis and nasal septal deviation, 17 non-atopic patients with nasal polyposis, and 13 atopic nasal polyp patients were enrolled in this cross-sectional study. Nasal secretion samples were collected a few days before surgery. The levels of IL-5 were measured using flow cytometry and the ECP using a commercial ELISA kit. In addition, we counted eosinophils in hematoxylin-and-eosin-stained sections of all nasal polyp and all nasal mucosa samples taken from the inferior nasal turbinates during septoplasty. A significantly higher concentration of IL-5 was found in the nasal fluid of atopic patients with nasal polyposis than in non-atopic nasal polyp patients (p=0.025) and patients with allergic rhinitis (p=0.05). ECP was higher in atopic nasal polyp patients than in patients with allergic rhinitis (p<0.0001) and than in non-atopic nasal polyp patients (p<0.0001). Polyp eosinophils were higher in atopic' than in non-atopic patients (p<0.0001) and higher than in the mucosa of patients with allergic rhinitis (p<0.0001). These however had significantly more mucosal eosinophils than was found in the polyps of non-atopic patients' (p=0.025). ECP levels in nasal fluid and eosinophil counts in tissue specimens correlated well in all three groups of patients. Our study has shown that atopic nasal polyp patients have a higher level of eosinophilic inflammation than non-atopic patients with nasal polyps and patients with allergic rhinitis.
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Feng, Zhaoxuan, Minglu Li, Xing Jin, et al. "Design and characterization of plasticized bacterial cellulose/waterborne polyurethane composite with antibacterial function for nasal stenting." Regenerative Biomaterials 7, no. 6 (2020): 597–608. http://dx.doi.org/10.1093/rb/rbaa029.
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Abstract A nasal stent capable of preventing adhesions and inflammation is of great value in treating nasal diseases. In order to solve the problems of tissue adhesion and inflammation response, we prepared plasticized bacterial cellulose (BCG) and waterborne polyurethane (WPU) composite with antibacterial function used as a novel nasal stent. The gelation behavior of BCG could contribute to protecting the paranasal sinus mucosa; meanwhile, the WPU with improved mechanical property was aimed at supporting the narrow nasal cavity. The thickness, size and the supporting force of the nasal stent could be adjusted according to the specific conditions of the nasal. Thermogravimetric analysis, contact angle and water absorption test were applied to investigate the thermal, hydrophilic and water absorption properties of the composite materials. The composite materials loaded with poly(hexamethylene biguanide) hydrochloride maintained well antibacterial activity over 12 days. Animal experiments further revealed that the mucosal epithelium mucosae damage of BCG−WPU composite was minor compared with that of WPU. This new type of drug-loaded nasal stent can effectively address the postoperative adhesions and infections while ensuring the health of nasal mucosal, and thus has an immense clinical application prospects in treating nasal diseases.
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Zhan, Yu, Lufang Tian, Ruxin Zhang, Shaoqing Yu, and Na Sun. "Ozone Induces Oxidative Stress and Inflammation in Nasal Mucosa of Rats." Atmosphere 15, no. 10 (2024): 1148. http://dx.doi.org/10.3390/atmos15101148.
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Background: The development of the global economy has led to changes in air pollution patterns. The haze phenomenon characterized by high concentrations of particulate matter 2.5 (PM2.5) has changed to complex pollution, and photochemical pollution characterized by ozone (O3) has become increasingly prominent. Ozone pollution and its impact on human health has become an important topic that needs to be studied urgently. Objective: To investigate the effects of ozone on oxidative stress and inflammation in the nasal mucosa of a rat model. Methods: Thirty-two healthy female Sprague–Dawley rats, eight in each group, were divided into four groups using the randomized numeric table method: normal control group (NC group), normal rats with a low level of ozone inhalation exposure (NEL group, 0.5 ppm), medium ozone inhalation exposure (NEM group, 1 ppm), and high ozone inhalation exposure (NEH group, 2 ppm). The ozone inhalation exposure groups were placed in the ozone inhalation exposure system and exposed to different concentrations of ozone for 2 h each day for 6 weeks. Nasal secretion was measured, and nasal lavage and nasal mucosa were collected. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) activities were measured by colorimetric assay, and the nasal mucosa was analyzed by Western blot. Western blot (WB) was used to detect the expression of NF-κB p65 nuclear protein in nasal mucosa. The mRNA expression of NF-κB target genes IL-6 and IL-8 and tumor necrosis factor-α (TNF-α) was detected by real-time quantitative PCR (qRT-PCR), and the protein content of pro-inflammatory factors IL-6, IL-8, and TNF-α was detected by ELISA in serum and nasal lavage fluid. The nasal mucosa of rats was stained with hematoxylin-eosin (HE) to observe the pathological changes in the nasal mucosa. The data were analyzed by SPSS 20.0 software. Results: The amount of nasal secretion increased significantly in all groups after ozone exposure compared with that in the NC group. The MDA content of the nasal mucosa was significantly increased in the ozone-exposed group compared with the NC group, and the activity levels of SOD and GSH-Px in the nasal mucosa were lower in the ozone-exposed group than in the NC group. The mRNA expression of IL-6, IL-8, and TNF-α in the nasal mucosa of the ozone-exposed group was elevated, and the protein content of TNF-α, IL-6, and IL-8 in the nasal lavage fluid was elevated, and the content increased with the increase in ozone concentration. The expression of NF-κB p65 intracellular protein in the nasal mucosa of each ozone-exposed group was higher than that of the normal group, and the content increased with the increase in ozone concentration. Conclusions: Ozone inhalation exposure promotes oxidative stress and the release of inflammatory factors TNF-α, IL-6, and IL-8, leading to pathological damage of the nasal mucosa, the degree of which increases with increasing concentration. This pathological process may be related to the activation of the transcription factor NF-κB by ozone in the nasal mucosa of rats, which increases the expression of its target genes.
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Piao, Chun Hua, Yan Jing Fan, Thi Van Nguyen, Chang Ho Song та Ok Hee Chai. "Mangiferin Alleviates Ovalbumin-Induced Allergic Rhinitis via Nrf2/HO-1/NF-κB Signaling Pathways". International Journal of Molecular Sciences 21, № 10 (2020): 3415. http://dx.doi.org/10.3390/ijms21103415.
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Mangiferin (MF), extracted from mango trees, is considered to have anti-inflammatory, anti-apoptotic, and antioxidant effects. However, its effects on allergic rhinitis (AR), remain unclear. We investigated the mechanisms underlying the protective action of MF in ovalbumin (OVA)-induced AR models. AR was induced by OVA challenge in BALB/c mice. Prior to this, MF and dexamethasone were administered. Mice were examined for nasal mucosal inflammation, the generation of allergen-specific cytokine response, and histopathological changes in the nasal mucosa and lung tissue. MF ameliorated nasal symptoms and nasal mucosa inflammation in OVA-induced AR and reduced inflammatory cell infiltration and epithelial disruption in these tissues. MF inhibited the overproduction of Th2/Th17 cytokines and transcription factors. MF downregulated the HO-1/Nrf2 pathways, reduced oxidative stress biomarker levels, and the NF-κB signaling pathways were inhibited. MF exerts protective effects in AR by inhibiting NF-κB and activating HO-1/Nrf2 pathways. MF could be used for the treatment of AR.
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Bui, Dan Van, Akira Kanda, Yoshiki Kobayashi, et al. "A Novel Approach for Investigating Upper Airway Hyperresponsiveness Using Micro-CT in Eosinophilic Upper Airway Inflammation such as Allergic Rhinitis Model." Biomolecules 9, no. 7 (2019): 252. http://dx.doi.org/10.3390/biom9070252.
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Airway hyperresponsiveness (AHR) has been proposed as a feature of pathogenesis of eosinophilic upper airway inflammation such as allergic rhinitis (AR). The measurement system for upper AHR (UAHR) in rodents is poorly developed, although measurements of nasal resistance have been reported. Here we assessed UAHR by direct measurement of swelling of the nasal mucosa induced by intranasal methacholine (MCh) using micro-computed tomography (micro-CT). Micro-CT analysis was performed in both naïve and ovalbumin-induced AR mice following intranasal administration of MCh. The nasal cavity was segmented into two-dimensional horizontal and axial planes, and the data for nasal mucosa were acquired for the region of interest threshold. Then, a ratio between the nasal mucosa area and nasal cavity area was calculated as nasal mucosa index. Using our novel method, nasal cavity structure was clearly identified on micro-CT, and dose-dependent increased swelling of the nasal mucosa was observed upon MCh treatment. Moreover, the nasal mucosa index was significantly increased in AR mice compared to controls following MCh treatment, while ovalbumin administration did not affect swelling of the nasal mucosa in either group. This UAHR following MCh treatment was completely reversed by pretreatment with glucocorticoids. This novel approach using micro-CT for investigating UAHR reflects a precise assessment system for swelling of the nasal mucosa following MCh treatment; it not only sheds light on the mechanism of AR but also contributes to the development of new therapeutic drugs in AR patients.
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Schulze, Gene E., Jim E. Proctor, Mark A. Dominick, et al. "Intranasal Toxicity of BMS-181885, A Novel 5-HT1 Agonist." International Journal of Toxicology 18, no. 5 (1999): 285–96. http://dx.doi.org/10.1080/109158199225206.
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One-month intranasal toxicity studies were conducted with BMS-181885 at doses of 1.5, 9, or 15 mg/animal/day in rats and 4, 24, or 40 mg/animal/day in monkeys. A 1-month intermittent intranasal toxicity study was also conducted in monkeys at doses of 3, 6, and 12 mg/animal 3 days per week. BMS-181885 was generally well tolerated in rats but resulted in dose-dependent nasal mucosal injury, primarily characterized by subacute inflammation of the nasal mucosa, and degeneration, single-cell necrosis, and/or erosion of the olfactory epithelium and, to a lesser extent, the respiratory epithelium. In monkeys, daily BMS-181885 administration was well tolerated and produced similar dose-dependent nasal injury primarily characterized by subacute inflammation of the nasal mucosa with degeneration and erosion of the olfactory epithelium. In a separate experiment, intermittent administration also resulted in dose-dependent nasal injury. In cultured rat nasal mucosal cells, BMS-181885 was toxic to olfactory epithelial cells with a range of mean IC50s between 44 and 291 μM. In contrast, BMS-181885 had no effect on respiratory epithelial cells up to its maximum solubility. Cytochrome P450 inhibition had no effect on the toxicity of BMS-181885 in olfactory epithelial cells but produced dose-dependent toxicity in respiratory epithelial cells, which was not present previously. The in vitro data suggest that parent drug, rather than a toxic metabolite, caused the drug-associated nasal mucosal injury.
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Mullol and Picado. "Endothelin in nasal mucosa: role in nasal function and inflammation." Clinical & Experimental Allergy 30, no. 2 (2000): 172–77. http://dx.doi.org/10.1046/j.1365-2222.2000.00754.x.
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Lee, Heung-Man, Hyo Yeol Kim, Hee Joon Kang, et al. "Up-Regulation of Protease-Activated Receptor 2 in Allergic Rhinitis." Annals of Otology, Rhinology & Laryngology 116, no. 7 (2007): 554–58. http://dx.doi.org/10.1177/000348940711600712.
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Objectives: We compared the patterns of PAR-2 messenger RNA (mRNA) and protein expression in the nasal mucosa of subjects with and without allergic rhinitis. Methods: Biopsy specimens were obtained from 10 patients with allergic rhinitis and 10 normal controls. RNA was extracted from the nasal mucosa, and semiquantitative reverse transcription-polymerase chain reaction was performed for PAR-2. Tissue sections were immunostained for PAR-2 by use of specific antibody. Results: The expression levels of PAR-2 mRNA in allergic rhinitis nasal mucosa were significantly up-regulated as compared with those in normal nasal mucosa. PAR-2 immunoreactivity was observed in the epithelium and submucosal glands in both normal controls and subjects with allergic rhinitis. Stronger immunoreactivity for PAR-2 was observed in allergic rhinitis nasal mucosa as compared with normal nasal mucosa. Conclusions: These results suggest that PAR-2 may be involved in allergic nasal inflammation.
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Migneault-Bouchard, C., F. J. M. Boselie, B. N. Landis, and J. Frasnelli. "Intranasal trigeminal sensitivity may be impaired after functional nasal surgery." Rhinology Online 5, no. 5 (2022): 8–9. http://dx.doi.org/10.4193/rhinol/21.049.
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Functional nasal surgery is frequently performed for sinonasal diseases not responding to medical treatment. Although surgery mostly turns out to be successful in such cases, a potential side effect of manipulating the nasal mucous membrane is impairment of intranasal trigeminal function. Not well known by specialists and clinically scarcely explored, this function provides sensory information from the nasal mucosa. It is responsible for the afferent part of protective nasal reflexes such as sneezing and coughing, but also provides the feeling of nasal airflow (1). Recent work suggests that patients with low intranasal trigeminal function are more prone to suffer from nasal obstruction and may be less satisfied with functional surgery (2-6). It has been suggested that intranasal trigeminal function decreases with mucosal changes, such as chronic inflammation and improves again once the inflammation has been treated (3). However, the influence of functional nasal surgery (i.e. surgery aimed at the improvement of nasal function) with consecutive mucosal micro-injuries on intranasal trigeminal function is not yet fully clear (2-4).
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Ceylan, Seyit Mehmet, Erdal Uysal, Mehmet Sokucu, et al. "The Effects of Halofuginone on Wound Healing in the Rat Nasal Mucosa." American Journal of Rhinology & Allergy 34, no. 1 (2019): 9–15. http://dx.doi.org/10.1177/1945892419866312.
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Background Halofuginone is an alkaloid febrifugine analogue and bioactive molecule that was isolated incidentally from the Dichroa febrifuga plant. The therapeutic efficacy of halofuginone in parasitic infections, scleroderma, inflammation, and fibrosis-related diseases, as well as in some types of cancer, has been previously reported. The effects of halofuginone on nasal mucosal damage are not yet known. Objective The aim of this study was to investigate the potential effect of topically applied halofuginone on wound healing in the mechanically injured nasal mucosa of rats. Methods A unilateral mucosal wound was created in the nasal cavity of 32 rats (aged 4 weeks) using the brushing technique. These rats were randomly divided into 4 groups. Although the control group did not receive an intervention, a dry pad, a saline-impregnated pad, or a pad impregnated with halofuginone were placed in the rats of the other 3 groups and left for 5 minutes. Rats were sacrificed on the 14th day, and a histological examination was performed. The nasal mucosa was assessed via hematoxylin-eosin and Masson’s trichrome staining. Results There were no statistically significant differences in epithelial thickness, inflammation, goblet cell formation, and epithelial disarray values between the halofuginone group and the control group ( P > .05). The subepithelial thickness was significantly decreased in the saline-treated group and the halofuginone-treated group ( P < .05), but a significantly lower level of subepithelial fibrosis was only observed in the halofuginone group compared to the other groups ( P < .05). Conclusions Topical halofuginone administration reduces the development of fibrosis and subepithelial edema after experimentally induced nasal mucosal injury, but it does not exert therapeutic or preventive effects on epithelial damage, inflammation, and goblet cell hyperplasia.
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Peric, Aleksandar, and Danilo Vojvodic. "Inflammatory mechanisms in nasal polyposis." Srpski arhiv za celokupno lekarstvo 142, no. 11-12 (2014): 740–46. http://dx.doi.org/10.2298/sarh1412740p.
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Nasal polyposis is a chronic inflammatory disease of the nasal and paranasal sinuses mucosa, characterized by prolaps of edematous mucosa, most commonly from the area of anterior ethmoid. The mean histological characteristics are proliferation of pseudostratified respiratory epithelium, thickening of the basement membrane, focal fibrosis and eosinophilic and lymphocytic infiltration of the lamina propria. Although etiology is unknown, two hypotheses are dominant among the scientists: ?hypothesis of staphylococcal superantigens? and ?hypothesis of immune barrier dysfunction?. Although we have not yet achieved a full understanding of the precise mechanisms underlying the pathogenesis of this disease, it is known that nasal polyposis is associated with intensive chronic inflammation, followed by dysregulation of chemotaxis, migration, activation and function of eosinophils. A great number of cytokines, chemokines, and adhesion molecules are involved in the regulation of these complex mechanisms. After activation, eosinophils produce and release enzymes, which can lead to the damage of mucosa and tissue remodeling. Hyperactive eosinophils release a new amount of chemokines and cytokines, attracting new eosinophils into the site of inflammation, and may cause the persistence of chronic inflammation.
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Wang, Sang, Lei Wang, Hua Hu, and Pin Dong. "MiR-224 ameliorates inflammation and symptoms in mouse model of allergic rhinitis by targeting CDK9." Allergologia et Immunopathologia 49, no. 6 (2021): 80–88. http://dx.doi.org/10.15586/aei.v49i6.451.
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Objectives To explore the regulatory effects of microRNA (miRNA)-224 and its potential target gene, cyclin dependent kinase 9 (CDK9), in the pathological process of allergic rhinitis (AR). Methods To investigate the role of miR-224 and CDK9, it was screened by bioinformatics prediction software and verified by dual-luciferase reporter assay. The mouse model of AR was established by ovalbumin (OVA).The animal models were intervened with miR-224 agomir, negative control agomir, and saline respectively. The symptoms of sneezing and nasal rubbing were recorded. The expressions of miR224, CDK9, and cytokines in the nasal mucosa of different groups were analyzed by rt-PCR or western blotting. Enzyme-linked immunoassay (ELISA) was used to evaluate the levels of IgE and Histamine (HA) in the serum. The infiltration of inflammatory cells in the nasal mucosa was studied by immunohistochemistry. The expression and distribution of CDK9 in the nasal mucosa of mice were revealed by immunofluorescence. Results In the nasal mucosa of the animal models, the level of miR-224 was downregulated, while that of CDK9 was upregulated. The upregulation of miR-224 by miR-224 agomir reduced the frequencies of nasal rubbing and sneezing, the expression of CDK9, the levels of cytokines, and the concentrations of IgE and HA. Moreover, miR-224 appeared to attenuate the infiltration of inflammatory cells and hypersecretion of glands in the nasal mucosa. The expression of CDK9, which was distributed under the mucosa, especially in the submucosa interstitial tissue, was significantly reduced. Conclusion MiR-224 affected the pathogenesis of AR by targeting CDK9. It proves that miR-224 could be a novel potential therapeutic target for AR.
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Rianto, Bambang Udji Djoko, Linggawati Kurniawan, and Kartono Sudarman. "The difference of nasal mucosal cytology features in gas station workers compared to non-gas station workers." Journal of the Medical Sciences (Berkala Ilmu Kedokteran) 51, no. 1 (2019): 63. http://dx.doi.org/10.19106/jmedsci005101201908.
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The pollutants contained in an outdoor air environment for example gasoline vapors can cause epithelial inflammation, metaplasia, and dysplasia. This study aimed to determine the difference in cytological nasal mucosa between gas station workers and non-gas station workers. This research used a cross-sectional design. There were 80 samples with inclusion criteria: aged 20-50 years, worked more than 3 months, consisting of 40 gas station workers (exposed group) and 40 non-gas station workers (unexposed group) who did not use nasal drops in the last ten days. The exclusion criteria of both groups were: 1) patients with acute rhinitis, 2) had nasal trauma, 3) had nasal surgery, 4) consume alcohol, 5) history of allergic rhinitis, and 6) refused to participate in the study. All samples performed brushing at 1/3 anterior nose inferior turbinate and cytology examination. The statistical analyses used X2 tests. From the exposed group we found 18 (45%) with inflammation, 17 samples (42.5%) with metaplasia, and 9 samples (22.5%) with dysplasia, while in the unexposed group there were 10 (20.5%) with inflammation, 4 (10.0%) with metaplasia and 2 (5.0%) dysplasia. There were statistically significant differences in nasal mucosal cytology, particularly metaplasia (p: 0.001; RP: 6.65; 95% CI: 1.78-27.01) and dysplasia (p: 0.023; RP: 5.52; 95% CI: 1.22-32.10) between both group samples. It can be concluded that there are statistically significant differences involving metaplasia and dysplasia in nasal mucosa cytology features of gas station workers compared to non-gas station workers.
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Perić, Aleksandar, Cveta Špadijer Mirković, and Danilo Vojvodić. "Clara cell protein 16 release from the nasal mucosa in allergic rhinitis, chronic rhinosinusitis, and exposure to air pollutants." Archives of Industrial Hygiene and Toxicology 69, no. 3 (2018): 215–19. http://dx.doi.org/10.2478/aiht-2018-69-3081.
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AbstractClara cell protein 16 (CC16) is a small protein mainly produced by non-ciliated Clara cells in the respiratory epithelium. It has an anti-inflammatory role in chronic upper and lower airway eosinophilic inflammations. Decreased levels of CC16 are found in the nasal secretions and plasma of patients with chronic eosinophilic inflammatory disorders, such as asthma, allergic rhinitis, and chronic rhinosinusitis with or without nasal polyps, as well as in people exposed to high levels of air pollutants. Intranasal corticosteroid administration suppresses chronic inflammation of the nasal mucosa driven by eosinophils and stimulates local CC16 production. CC16 can be a reliable biomarker of the beneficial effects of perennial allergic rhinitis and chronic rhinosinusitis therapy and of the functional recovery of the nasal mucosa after treatment with topical glucocorticoids.
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Woś, Jan, and Agnieszka Remjasz. "Inflammation of the nasal mucosa and paranasal sinuses." Polski Przegląd Otorynolaryngologiczny 8, no. 1 (2019): 15–24. http://dx.doi.org/10.5604/01.3001.0013.1412.
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Inflammation of the paranasal sinuses is a common condition that affects the upper respiratory tract. The pathomechanism and course of sinusitis are multifaceted, depending on the etiological factors, duration of the disease, anatomical abnormalities, and additional conditions exacerbating the inflammation of the nasal mucosa and paranasal sinuses. The gold standard of diagnostic imaging is computed tomography (CT), performed in particular cases. An auxiliary examination is a magnetic resonance imaging (MRI) for soft tissue imaging when there is a suspicion of a neoplastic process. The treatment of patients with rhinosinusitis is very complex and long-lasting, associated with the use of nasal or systemic corticosteroids, irrigation with physiological saline, as well as antibiotic therapy, antihistamines or herbal supplements. The treatment is selected individually for the patient's condition or the sinus phenotype, and in exceptional cases, surgical intervention is undertaken. Work is continuing on genetic, molecular and immunological research to search for new and effective methods of treatment of rhinosinusitis.
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Zoabi, Yara, Francesca Levi-Schaffer, and Ron Eliashar. "Allergic Rhinitis: Pathophysiology and Treatment Focusing on Mast Cells." Biomedicines 10, no. 10 (2022): 2486. http://dx.doi.org/10.3390/biomedicines10102486.
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Allergic rhinitis (AR) is a common rhinopathy that affects up to 30% of the adult population. It is defined as an inflammation of the nasal mucosa, develops in allergic individuals, and is detected mostly by a positive skin-prick test. AR is characterized by a triad of nasal congestion, rhinorrhea, and sneezing. Mast cells (MCs) are innate immune system effector cells that play a pivotal role in innate immunity and modulating adaptive immunity, rendering them as key cells of allergic inflammation and thus of allergic diseases. MCs are typically located in body surfaces exposed to the external environment such as the nasal mucosa. Due to their location in the nasal mucosa, they are in the first line of defense against inhaled substances such as allergens. IgE-dependent activation of MCs in the nasal mucosa following exposure to allergens in a sensitized individual is a cardinal mechanism in the pathophysiology of AR. This review is a comprehensive summary of MCs’ involvement in the development of AR symptoms and how classical AR medications, as well as emerging AR therapies, modulate MCs and MC-derived mediators involved in the development of AR.
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Zamfir-Chiru-Anton, Adina, and Dan-Cristian Gheorghe. "Potential markers for allergic rhinitis evaluation." Romanian Medical Journal 63, no. 1 (2016): 17–19. http://dx.doi.org/10.37897/rmj.2016.1.4.
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Allergic rhinitis is the result of a permanent/intermitent inflammation of the nasal mucosa, exposed to certain alergens. An immunological reaction is the fundamental cause – a type I hypersensitivity reaction, followed by local inflammatory response and immune cell pooling (eosinophiles, basophiles, Th cells, mast cells) in the nasal mucosa. Matrix metaloproteinases are tissue proteases that degrade extracellular matrix and basilar membrane and modulate immune responses. Our article reviews the part metalloproteinases play in the changes suffered by the nasal mucosa in chronic allergic rhinitis (fibrosis, metaplasia, edema, inflammatory cell infiltration).
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Larsen, Per L., Peter K. Tingsgaard, Jonathan Harcourt, Gitte Sofsrud, and Mirko Tos. "Nasal Polyps and Their Relation to Polyps/Hypertrophic Polypoid Mucosa in the Paranasal Sinuses: A Macro-, Endo-, and Microscopic Study of Autopsy Materials." American Journal of Rhinology 12, no. 1 (1998): 45–52. http://dx.doi.org/10.2500/105065898782103052.
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The present study comprised macro- and endoscopic screening of the nasosinusal complex in 56 autopsies, 24 with nasal polyps and 32 without. Seven had nasal polyposis (bilaterally more than two). Hypertrophic polypoid mucosa in the paranasal sinuses was not found in the cases with nasal polyposis and in only 2 (4%) of the total number (24) of cases with polyps. Microscopic examination of nine small polyps, the mucosa from which they originated, and control specimens showed accumulation of eosinophils in the mucosa from which the polyps originated, indicating localized inflammation.
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Nagata, Yoshiyuki, Shuichiro Maruoka, Yasuhiro Gon, et al. "Expression of IL-25, IL-33, and Thymic Stromal Lymphopoietin in Nasal Polyp Gland Duct Epithelium in Patients With Chronic Rhinosinusitis." American Journal of Rhinology & Allergy 33, no. 4 (2019): 378–87. http://dx.doi.org/10.1177/1945892419835333.
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Background Nasal polyps accompany eosinophilic chronic rhinosinusitis (ECRS). Cytokines, including interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP) expressed in nasal mucosa have been implicated in polyp pathogenesis. We investigated the role of nasal polyp epithelium cytokine expression in eosinophilic infiltration in ECRS. Methods Tissues were collected from 39 patients undergoing nasal surgery. Cases were divided into 3 groups: control (CTR), non-ECRS (nECRS), and ECRS and were evaluated for IL-25, IL-33, and TSLP expression. Results Abundant eosinophilia was observed underneath the nasal mucosa and around the nasal ducts in polyps in ECRS and correlated positively with IL-33 protein expression. Conclusion Cytokine expression in nasal duct cells and eosinophilic infiltration around duct cells similar to those in the nasal mucosa occurred in the nasal epithelium of polyps, suggesting its role in inducing eosinophilic inflammation.
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Svensson, Christer, Morgan Andersson, Lennart Greiff, and Carl G. A. Persson. "Nasal Mucosal Endorgan Hyperresponsiveness." American Journal of Rhinology 12, no. 1 (1998): 37–44. http://dx.doi.org/10.2500/105065898782103016.
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Nonspecific hyperresponsiveness of the upper and lower airways is a well-known characteristic of different inflammatory airway diseases but the underlying mechanisms have not yet been satisfactorily explained. In attempts to elucidate the relation of hyperresponsiveness to disease pathophysiology we have particularly examined the possibility that different airway endorgans may alter their function in allergic airway disease. The nose, in contrast to the bronchi, is an accessible part of the airways where in vivo studies of airway mucosal processes can be carried out in humans under controlled conditions. Different endorgans can be defined in the airway mucosa: subepithelial microvessels, epithelium, glands, and sensory nerves. Techniques may be applied further in the nose to determine selectively the responses/function of these endorgans. Topical challenge with methacholine will induce a glandular secretory response, and topical capsaicin activates sensory c-fibers and induces nasal smart. Topical histamine induces extravasation of plasma from the subepithelial microvessels. The plasma exudate first floods the lamina propria and then moves up between epithelial cells into the airway lumen. This occurs without any changes in the ultrastructure or barrier function of the epithelium. We have therefore forwarded the view of mucosal exudation of bulk plasma as a physiological airway tissue response with primarily a defense function. Since the exudation is specific to inflammation, we have also suggested mucosal exudation as a major inflammatory response among airway endorgan functions. Using a “nasal pool” device for concomitant provocation with histamine and lavage of the nasal mucosa we have assessed exudative responses by analyzing the levels of plasma proteins (e.g., albumin, α2-macroglobulin) in the returned lavage fluids. A secretory hyperresponsiveness occurs in both experimental and seasonal allergic rhinitis. This type of nasal hyperreactivity may develop already 30 minutes after allergen challenge. It is attenuated by topical steroids and oral antihistamines. We have demonstrated that exudative hyperresponsiveness develops in both seasonal allergic rhinitis and common cold, indicating significant changes of this important microvascular response in these diseases. An attractive hypothesis to explain airway hyperresponsiveness has been increased mucosal absorption permeability due to epithelial damage, possibly secondary to the release of eosinophil products. However, neither nonspecific nor specific endorgan hyperresponsiveness in allergic airways may be explained by epithelial fragility or damage since nasal absorption permeability (measured with 51Cr-EDTA and dDAVP) was decreased or unchanged in our studies of allergic and virus-induced rhinitis, respectively. Thus, the absorption barrier of the airway mucosa may become functionally tighter in chronic eosinophilic inflammation.
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Chen, Langlang, Xin Fan, Lina Yang, Lu Han, Ningbo Wang, and Ka Bian. "Research progress of glucocorticoid resistance in chronic rhinosinusitis with nasal polyps: A review." Medicine 102, no. 46 (2023): e36024. http://dx.doi.org/10.1097/md.0000000000036024.
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Chronic rhinosinusitis with nasal polyps (CRSwNP) is one of the common chronic inflammatory diseases in otolaryngology. Glucocorticoid (GC) acts as the first-line drug for the treatment of CRSwNP in clinical practice, and they play an irreplaceable role in reducing nasal mucosal inflammation and restoring the normal physiological function of the nasal mucosa. However, many patients are still insensitive to GC treatment, known as GC resistance, which leads to poor control of the disease, and the underlying mechanisms are still not fully elucidated. This article provides a comprehensive overview of the research progress of GC resistance of patients with CRSwNP in recent years.
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Jiang, Liang, Dianzhong Liu, and Xiaoyan Hu. "Effects of Lactobacillus on Interleukin-4 (IL-4), Tumour Necrosis Factor-Alpha (TNF-Alpha) and Immune Function in Allergic Rhinitis Rats." Journal of Biomaterials and Tissue Engineering 12, no. 1 (2022): 221–25. http://dx.doi.org/10.1166/jbt.2022.2878.
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Allergic rhinitis (AR) is a type of nasal mucosal inflammation. Lactobacillus plays a critical role in maintaining micro-ecological balance. This study aims to detect its effects on IL-4, TNF-α, Th1 and Th2 in AR sprapue-dawley (SD) rat after lactobacillus intervention. Ovalbumin (OVA) allergic AR SD rat model was established and assigned into model group, experimental group and blank group followed by analysis of Nasal mucosa under the microscope, IL-4 and TNF-α level by ELISA and immunohistochemistry assay, and Th1 and Th2 cells in spleen by flow cytometry. AR symptom in experimental group was significantly severe compared to blank group, but relative better compared to model group (p < 0.05). Nasal mucosal hyperemia and inflammation was significantly ameliorated in experimental group with significantly increased Th1 cells and Th1/Th2 ratio and decreased Th2 cells compared to model group (p < 0.05). In conclusion, Lactobacillus intervention reduced IL-4 and TNF-α expression in serum and tissue and ameliorated the inflammation in AR rat.
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Tyrnova, E. V. "HUMAN BETA-DEFENSIN-3 GENE EXPRESSION IN THE NASAL AND SINONASAL MUCOSA." Medical academic journal 19, no. 1S (2019): 184–86. http://dx.doi.org/10.17816/maj191s1184-186.
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Sensitive receptors of the olfactory sensory system are located in the nasal cavity mucosa. The aim of this study was to evaluate the human beta-defensin-3 (hBD-3) gene expression in the surface epithelium of the nasal and sinonasal mucosa. Surgical samples from patients with nasal and sinonasal disease (n = 85) (sinus maxillaries mucosa, choana polyps, middle nasal passage polyps, sinus maxillaries polyps, inferior turbinate mucosa of hypertrophic rhinitis, inferior turbinate mucosa and the middle nasal passage mucosa as controls) were investigated. Total RNA was extracted and analysed by real-time RT-PCR for hBD-3 as well as beta-actin mRNA.hBD-3 gene expression was detected in all examined anatomical regions in 14.29-33.33% samples at low levels, but it was absent in the hypertrophic inferior turbinate mucosa (Fisher’s exact test, p < 0.05 compared to the middle nasal passage mucosa; p < 0.01, odds ratio (OR) 31.15, 95% confidence interval (CI) 1.53÷633.6 compared to the middle nasal passage polyps). The highest hBD-3 mRNA expression detection frequency was detected in the middle nasal passage polyps (53.84% cases) (p < 0.05, OR 7.00, CI 1.10÷44.63 compared to the sinus maxillaries mucosa). The highest levels of hBD-3 gene expression was detected in the middle nasal passage polyps also (Wilcoxon signed rank test, p < 0.05 compared to the hypertrophic inferior turbinate mucosa). Clinically, inflammatory polyps are found in the middle turbinate in patients with chronic rhinosinusitis but not in the inferior turbinate. In the context of chronic inflammation, apart from direct antimicrobial activity, high concentrations hBD-3 also potentially contributes to epithelial injury and fibrotic remodeling.
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Huriyati, Effy, Eryati Darwin, Yanwirasti Yanwirasti, and Irza Wahid. "Association of Inflammation Mediator in Mucosal and Tissue of Chronic Rhinosinusitis with Recurrent Nasal Polyp." Open Access Macedonian Journal of Medical Sciences 7, no. 10 (2019): 1635–40. http://dx.doi.org/10.3889/oamjms.2019.327.
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BACKGROUND: Chronic rhinosinusitis with polyps (CRSwNP) have a high risk of recurrence and patients often experience repeated surgery. There are several types of inflammatory patterns in CRSwNP, such as Th2 inflammation (eosinophilic) and Th1/Th17 inflammation (neutrophilic).
 AIM: This study aims to determine the expression of IL-5, IL-8, IL-17A and TGF-β in recurrent CRSwNP using the most convenient and non-invasive examination tool such as brushing the mucosal polyp and find out its correlation with polyp tissues.
 MATERIAL AND METHODS: A cross-sectional comparative study was carried out on 15 samples of mucosal brushing and polyp tissue. Expressions of IL-5, IL-8, IL-17A and TGF-β on mucosa were measured using the Enzyme-Linked Immunosorbent Assay (ELISA) examination and tissues using Immunohistochemical (IHC) examination.
 RESULT: The result showed that Only IL-5 has a significant relationship between mucosa and tissue with moderate positive correlation (p < 0.05; r = 0.527).
 CONCLUSION: This study concluded that mucosa brushing could be used as a simple and non-invasive examination to observe the expression of IL-5 in recurrent CRSwNP. IL-5 is one of the cytokines that mark the Th2 (eosinophilic) inflammatory pattern where eosinophilic polyps are closely related to recurrence.
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Pyun, Bo-Jeong, Kyuhyung Jo, Joo Young Lee, et al. "Caesalpinia sappan Linn. Ameliorates Allergic Nasal Inflammation by Upregulating the Keap1/Nrf2/HO-1 Pathway in an Allergic Rhinitis Mouse Model and Nasal Epithelial Cells." Antioxidants 11, no. 11 (2022): 2256. http://dx.doi.org/10.3390/antiox11112256.
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Allergic rhinitis (AR) is a common upper-airway inflammatory disease of the nasal mucosa caused by immunoglobulin (IgE)-mediated inflammation. AR causes various painful clinical symptoms of the nasal mucosa that worsen the quality of daily life, necessitating the urgent development of therapeutic agents. Herein, we investigated the effects of Caesalpinia sappan Linn. heartwood water extract (CSLW), which has anti-inflammatory and antioxidant properties, on AR-related inflammatory responses. We examined the anti-inflammatory and anti-allergic effects of CSLW in ovalbumin (OVA)-induced AR mice and in primary human nasal epithelial cells (HNEpCs). Administration of CSLW mitigated allergic nasal symptoms in AR mice, decreased total immune cell and eosinophil counts in nasal lavage fluid, and significantly reduced serum levels of OVA-specific IgE, histamine, and Th2 inflammation-related cytokines. CSLW also inhibited the infiltration of several inflammatory and goblet cells, thereby ameliorating OVA-induced thickening of the nasal mucosa tissue. We found that CSLW treatment significantly reduced infiltration of eosinophils and production of periostin, MUC5AC, and intracellular reactive oxygen species through the Keap1/Nrf2/HO-1 pathway in HNEpCs. Thus, our findings strongly indicate that CSLW is a potent therapeutic agent for AR and can improve the daily life of patients by controlling the allergic inflammatory reaction of the nasal epithelium.
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Chiarella, Emanuela, Nicola Lombardo, Nadia Lobello, et al. "Deficit in Adipose Differentiation in Mesenchymal Stem Cells Derived from Chronic Rhinosinusitis Nasal Polyps Compared to Nasal Mucosal Tissue." International Journal of Molecular Sciences 21, no. 23 (2020): 9214. http://dx.doi.org/10.3390/ijms21239214.
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Chronic rhinosinusitis of the nasal mucosa is an inflammatory disease of paranasal sinuses, which causes rhinorrhea, nasal congestion, and hyposmia, and in some cases, it can result in the development of nasal polyposis. Nasal polyps are benign lobular-shaped growths that project in the nasal cavities; they originate from inflammation in the paranasal mucous membrane and are associated with a high expression of interleukins (IL)-4, IL-5, IL-13, and IgE. Polyps derive from the epithelial–mesenchymal transition of the nasal epithelium resulting in a nasal tissue remodeling. Nasal polyps from three patients with chronic rhinosinusitis as well as control non-polyp nasal mucosa were used to isolate and cultivate mesenchymal stem cells characterized as CD73+, CD90+, CD105+/CD14−, CD34−, and CD45−. Mesenchymal stem cells (MSCs) cultures were induced to differentiate toward adipocytes, where lipid droplets and adipocyte genes PPARγ2, ADIPO-Q, and FABP4 were observed in control non-polyp nasal mucosa-derived mesenchymal cells but were scarcely present in the cultures derived from the nasal polyps, where apoptosis was evident. The modulation of the response to adipogenic stimulus in polyps represents a change in the molecular response that controls the cascade required for differentiation as well as possible means to specifically target these cells, sparing the normal mucosa of the nasal sinuses.
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Iskhakova Fotima Sharifovna. "Treatment of Allergic Rhinitis by Modern Methods from the Point of View of a Doctor: The Main Problems and Mistakes." Texas Journal of Medical Science 18 (March 22, 2023): 52–56. http://dx.doi.org/10.62480/tjms.2023.vol18.pp52-56.
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Allergic rhinitis (AR) is a chronic pathological process, the main pathogenetic mechanism of which is inflammation caused by immunoglobulin E (IgE)–an indirect hypersensitivity reaction that develops as a result of allergens entering the nasal mucosa and manifesting sneezing, nasal congestion, itching and nasal discharge of various nature.
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Duda, Roxana. "The role of inflammatory mediators in the pathogenesis of nasal polyposis: Literature review." Romanian Journal of Rhinology 5, no. 18 (2015): 81–85. http://dx.doi.org/10.1515/rjr-2015-0009.
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AbstractNasal polyposis represents a late stage of long-lasting inflammation of the sinonasal mucosa, characterized by increased inflammatory cells infiltration and anomalous tissue remodelling. A wide range of chemical mediators such as cytokines, chemokines, cell adhesion molecules are involved in the pathomechanism of nasal polyposis, but their significance has not been completely clarified.Eosinophils are the dominant inflammatory cell population in nasal polyposis and are thought to be the central effector cells responsible for the onset and maintenance of the inflammatory process. Persistent inflammation of the sinonasal mucosa can lead to structural changes, such as epithelial damage, thickened basement membrane, stromal edema, formation of pseudocysts. This review summarizes prior and current knowledge regarding the involvement of the inflammatory process in the pathogenesis of nasal polyposis.
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Rogers, D. F. "Reflexly runny noses: neurogenic inflammation in the nasal mucosa." Clinical & Experimental Allergy 26, no. 4 (1996): 365–67. http://dx.doi.org/10.1111/j.1365-2222.1996.tb00550.x.
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CAPELLIER, G., Z. ZHANG, M. F. MAHEU, et al. "Nasal mucosa inflammation induced by oxygen administration in humans." Acta Anaesthesiologica Scandinavica 41, no. 8 (1997): 1011–16. http://dx.doi.org/10.1111/j.1399-6576.1997.tb04828.x.
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Rogers, D. F. "Reflexly runny noses: neurogenic inflammation in the nasal mucosa." Clinical Experimental Allergy 26, no. 4 (1996): 365–67. http://dx.doi.org/10.1046/j.1365-2222.1996.d01-332.x.
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Shima, Tetsuya. "Lipoxygenase Metabolites in Chronic Inflammation of the Nasal Mucosa." Practica oto-rhino-laryngologica. Suppl. 1988, Supplement26 (1988): 1–14. http://dx.doi.org/10.5631/jibirinsuppl1986.1988.supplement26_1.
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Begvarfaj, Elona, Emilio Greco, Arturo Armone Caruso, et al. "Effects of the Silica Dust on the Nasal Mucosa of Ceramic Workers." Sustainability 14, no. 19 (2022): 12556. http://dx.doi.org/10.3390/su141912556.
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Background. Adverse health effects due to occupational exposures are a global public health concern and have been studied for many years. Ceramic workers are occupationally exposed to a wide range of toxic substances as they manage clay (silico-aluminous feldspar mixed with sodium, potassium salts and iron oxide). The objective of this study was to assess the presence of any inflammation or alteration of the nasal mucosa of ceramic workers by nasal cytology. Materials and methods. Twenty-eight ceramic workers from Caltagirone (Italy) were enrolled. Nasal symptoms, atopy, health habits and workplace features were assessed by a special questionnaire, and nasal mucosa health was evaluated by nasal cytology. Results. The cytological study of the nasal mucosa revealed the constant presence of abundant, thick and filamentous mucus, as well as a reorganization of the nasal cellularity with a prevalence of muciparous hyperplasia and metaplasia in the study group, and only in a lesser extent for the subjects with some protective environmental measures. Conclusions. The ceramic workers showed chronic inflammatory rhinitis on nasal cytology, with a remodelling of the nasal mucosa and thick mucus. Nasal cytology may be a helpful tool either for the health surveillance of the ceramic workers, or for the screening of any pathology of the upper airways.
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Briles, David E., Lea Novak, Muneki Hotomi, Frederik W. van Ginkel, and Janice King. "Nasal Colonization with Streptococcus pneumoniae Includes Subpopulations of Surface and Invasive Pneumococci." Infection and Immunity 73, no. 10 (2005): 6945–51. http://dx.doi.org/10.1128/iai.73.10.6945-6951.2005.
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ABSTRACT We demonstrated that during colonization with Streptococcus pneumoniae the nasal mucosal tissues of mice support two populations of pneumococci. Transparent-phase pneumococci can be readily washed from the outer surface, while a second population composed of primarily opaque-phase pneumococci is released only by homogenization of the nasal tissue. The fact that the opaque phase has previously been associated with invasion and the fact that opaque-phase pneumococci were released by homogenization of previously washed nasal tissue suggest that the opaque-phase pneumococci may have invaded the nasal tissue. Consistent with this hypothesis was our observation that there was inflammation in portions of the nasal mucosa of the colonized mice but not in the mucosa of noncolonized mice, but this observation did not prove the hypothesis. If the opaque-phase pneumococci released from the nasal tissue were from within the tissue and/or if resistance of the opaque-phase subpopulation to antibody, complement, and phagocytes is essential for long-term carriage, it seems likely that the virulence factors of S. pneumoniae that are necessary for killing humans exist to facilitate carriage. Although this speculation is unproven, the observation that there are separate populations of pneumococci during colonization may help guide future attempts to understand the biology of nasal colonization by this pathogen.
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Sarkar, Saurav, Fabien Magne, Giriprasad Venugopal, et al. "Altered Nasal Microbiome in Atrophic Rhinitis: A Novel Theory of Etiopathogenesis and Therapy." Microorganisms 10, no. 11 (2022): 2092. http://dx.doi.org/10.3390/microorganisms10112092.
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Background: Atrophic rhinitis (AtR) is a chronic nasal condition with polygenic and polybacterial etiology. We investigated the clinical outcomes of honey therapy and the associated nasal microbiome in AtR. Methods: For eight weeks, a nonrandomized control trial using a nasal spray of 10% manuka honey and saline on the right and left sides of the nose was conducted on 19 primary AtR patients. A nasal endoscopy was performed and a mucosal biopsy were taken before and after the intervention. Five of the nineteen patients were selected for microbiome and GPR43 expression studies. Results: We used manuka honey to describe an effective prebiotic treatment for atrophic rhinitis. There were nine males and ten females with an average (±SD) age of 33.8 (±10.7) years. Endoscopic scores and clinical symptoms improved in honey-treated nasal cavities (p < 0.003). There was a significant decrease in inflammation, restoration of mucus glands, and increased expression of GPR43 in the nasal cavities with honey therapy. The nasal microbiome composition before and after treatment was documented. Particularly, short chain fatty acid (SCFA) producers were positively enriched after honey therapy and correlated with improved clinical outcomes like nasal crusting, congestion, and discharge. Conclusion: Our approach to treating AtR patients with manuka honey illustrated effective clinical outcomes such as (1) decreased fetid smell, (2) thickening of the mucosa, (3) decreased inflammation with healed mucosal ulcers, (4) increased concentration of the mucosal glands, (5) altered nasal microbiome, and (6) increased expression of SCFA receptors. These changes are consequent to resetting the nasal microbiome due to honey therapy.
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Paranjpe, Madhav G., Jessica L. Belich, Dayauna R. Richardson, et al. "Exudative Inflammatory Lesions in the Nasal Cavities of the 26-Week Tg.rasH2 Mice Oral Gavage Carcinogenicity Studies." International Journal of Toxicology 36, no. 1 (2016): 21–28. http://dx.doi.org/10.1177/1091581816673583.
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Three levels of nasal cavity sections (anterior, middle, and most posterior) are routinely examined as protocol required tissues in our 26-week carcinogenicity studies involving Tg.rasH2 mice. Exudative inflammation of the nasal cavity was noted in the most posterior section of both males and females that were administered vehicle and/or test article via oral gavage, particularly when the vehicle and/or test article had irritant properties, was in the form of a salt, had a low pH, and/or was viscous. The exudative inflammatory lesion was characterized by the presence of eosinophilic proteinaceous fluid, fibrin, mucin, sloughed cells, and degenerate neutrophils within the nasal cavities. In lesions of increased severity, there was often degeneration, necrosis, and erosion of the underlying mucosa. Often, there was hyperplasia as well as squamous metaplasia of the mucosa. Retrospective analysis of our data, involving thirty-two 26-week Tg.rasH2 carcinogenicity studies, revealed that despite the presence of these exudative inflammatory changes with degeneration, necrosis, and mucosal hyperplasia, progression to tumor formation in the nasal cavities was rare and the incidence of nasal tumors was comparable in animals with or without exudative inflammatory lesions.
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Bui, Thi Tho, Chun Hua Piao, Eunjin Hyeon, et al. "Preventive Effect of Bupleurum chinense on Nasal Inflammation via Suppressing T Helper Type 2, Eosinophil and Mast Cell Activation." American Journal of Chinese Medicine 47, no. 02 (2019): 405–21. http://dx.doi.org/10.1142/s0192415x19500204.
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Bupleurum chinense is distributed in East Asia and has been used as a traditional herbal medicine for more than a thousand years. Though B. chinense has been reported to have immunomodulatory, anti-inflammatory, anti-oxidant, hepato-protective, antipyretic, analgesic and antifibrotic effects, its specific effect on allergic rhinitis disease has not been clarified. In this study, we investigated the anti-allergic and anti-inflammation effects of B. chinense extract (BCE) in an ovalbumin (OVA)-induced allergic rhinitis (AR) mouse model. Oral administration of BCE in a dose-independent manner regulated the balance of Th1/Th2/Treg cell differentiation in AR mice. Accordingly, BCE attenuated the expression of Th2-related cytokines such as IL-4, IL-5 and IL-13 in nasal lavage fluid (NALF) and nasal tissue and up-regulated the secretion of Th1/Treg cells including IL-10, IL-12 and IFN-[Formula: see text]. Also, BCE inhibited the formation and migration of eosinophils to the nasal mucosa and NALF, as well as suppressed CCL24, an eosinophil-specific chemoattractant in NALF. The levels of anti-OVA specific IgE and anti-OVA specific IgG1 were decreased, and as a result, the allergic response was attenuated by BCE via inhibiting mast cells accumulation in nasal mucosa and serum histamine release. The nasal allergy symptoms, nasal mucosal swelling, epithelial barrier disruption and mucus hyperplasia were obviously ameliorated. These results suggest that BCE may have therapeutic potential for treating allergic rhinitis through modulating the accumulation and activation of important leukocytes in the immune system such as Th1, Th2, Treg, eosinophils and mast cells.
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Krasil’nikova, S. V., T. I. Eliseeva, E. V. Tush, E. V. Bol’shova, N. I. Kubysheva, and I. I. Balabolkin. "Features of local inflammation of nasal mucosa in children with bronchial asthma." Russian Otorhinolaryngology 19, no. 3 (2020): 22–30. http://dx.doi.org/10.18692/1810-4800-2020-3-22-30.
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Bronchial asthma (BA) is often associated with chronic inflammatory processes in the nasal mucosa; these processes give rise to allergic rhinitis (AR), chronic rhinosinusitis, adenoiditis and polypous rhinosinusitis. Due to their multiple symptoms, these diseases of the upper respiratory tract, especially allergic rhinitis, are often difficult to verify in patients with asthma. The aim of the study was to assess the features of local inflammation of the nasal mucosa in patients with BA and AR. Patients and methods. 93 children with BA were examined. General clinical, allergological, functional examination, measurement of endonasal temperature and determination of IgE and IL4 content in nasal secretions were performed. Results. Children with BA have lower values of endonasal temperature than healthy ones. There was a tendency to decrease endonasal temperature as the symptoms of AR increased. In the acute stage of AR, the temperature values were lower than in the remission stage, р = 0,02. The addition of infectious inflammation of the nasal mucosa in children with AD was accompanied by an increase in endonasal temperature, р = 0,04. The increase of the content of nasal IgE in acute AR – 115,6 (49,9; 181,2) ME/mg, compared to the remission period to 24,9 (6,2; 43,7) ME/mg. Exacerbation of AR was associated with increased IL4 to 109,7 (54,2; 165,2) PG/mg, in the period of remission – 34,4 (12,0; 56,8) PG/mg. The increase of these biomarkers of allergic inflammation have a correlative relationship, R = 0,44, p = 0,002. The relationship of IL4 content with endonasal temperature, R = 0,44 р = 0,02 was established. Conclusion. Patients with BA and AR showed a decrease in endonasal temperature compared to healthy ones. Exacerbation of AR in children with BA characterized by an increase in the content of nasal IgE and IL4 and a decrease in endonasal temperature, which allows us to consider these indicators as biomarkers of activation of allergic inflammation.
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Perkins, Jonathan A., Katherine H. Moore, Domenic M. Canonico, and Michael R. Morris. "Neuropeptide Levels in the Nasal Secretion and Nasal Mucosa of Patients with Chronic Sinusitis and Nasal Polyposis." American Journal of Rhinology 8, no. 3 (1994): 117–22. http://dx.doi.org/10.2500/105065894781874377.
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Neuropeptides are present within the nasal cavity and are thought to mediate inflammation in this region. The exact role these peptides might play in causing the inflammation present in chronic rhinosinusitis and nasal polyposis is not known. Calcitonin Gene Related Peptide (CGRP) was measured in the nasal secretion and nasal mucosa of 10 patients having chronic rhinosinusitis and 10 patients with nasal polyposis, using radioimmunoassay. These values were compared to ten controls without sinonasal disease. Additionally, each subject's history and baseline laboratory data were analyzed to establish the presence or absence of allergic disease. The results of these assays are discussed, as well as the potential pathophysiologic role that neuropeptides play in these disease states.
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Tyrnova, E. V., G. M. Aleshina та Yu K. Yanov. "Human β-defensin-3gene expression in mucosa of ORL organs". Medical Immunology (Russia) 24, № 4 (2022): 779–92. http://dx.doi.org/10.15789/1563-0625-hbd-2384.
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The aim of present study was to investigate the hBD-3 gene expression in the surface epithelium of mucosa in ORL organs. We have studied a total of 210 mucosal samples, obtained at the most frequent surgical intervantions from 5 different anatomical functional areas: nose and paranasal sinuses, middle ear, nasopharynx, oropharynx, larynx. The inferior turbinate mucosa (1) and the normal middle nasal passage mucosa (2) served as controls. Estimation of hBD-3 and β-actin gene expression was performed by reverse transcription and realtime PCR. In the nasal and sino-nasal mucosa, only negligible expression levels were detected in 14.29-33.33% of samples, most often in the specimens from the middle nasal passage and ethmoid labyrinth polyps (53.84%), being absent in hypertrophic inferior turbinate. In the middle ear cavity, the frequency detection of the hBD-3 gene expression varied from 7.69% in the stapes superstructures mucosa to 53.85% of the mucosal samples in the presence of cholesteatoma. hBD-3 gene expression was detected in most tissue samples with high microbial contamination: palatine tonsils (100%); adenoid hypertrophy (84.62%); adenoids in hypertrophic states of adenoids and palatine tonsils (87.5%); laryngeal fibrous-vascular polyps (87.5%); other laryngeal pathology (77.78% of the samples). The highest levels of hBD-3 gene expression were found in laryngeal fibrous-vascular polyps. The findings presumed two functionally different types of immune response in mucosa of the ORL organs. In the anatomical-functional areas lined with ciliated epithelium (middle and inferior nasal passages, maxillary and ethmoid sinuses, middle ear), significantly lower frequencies (Fisher's exact test, p < 0.05 to p < 0.001) and levels (Mann-Whitney test, p < 0.05 to p < 0.001) of hBD-3 gene expression were detected, except of polyps of the middle nasal passage and ethmoid labyrinth, and mucosa of the tympanic cavity in cholesteatoma, which may be related to the nature of the pathological process. In the areas lined with squamous epithelium or a combination of squamous and ciliated epithelium, hBD-3 gene expression was detected almost everywhere and at significantly higher levels. In the context of chronic inflammation and infection-related diseases of the ORL organs, in addition to the direct microbicidal activity of hBD-3 as the first line of immune response, one may suggest peptide dysregulation and, even, pathogenetic effects of hBD-3, e.g., increased sensitivity to infections, pathological changes in the composition of the commensal bacteria, fibrous remodeling.
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Naik, Mahendra S., and Sulabha M. Naik. "An Unusual Presentation of Nasal Polyp Arising from Floor of Nasal Cavity." An International Journal of Otorhinolaryngology Clinics 3, no. 2 (2011): 129–31. http://dx.doi.org/10.5005/jp-journals-10003-1071.
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ABSTRACT Introduction Nasal polyps are pedunculated, edematous, prolapsed mucosa of the paranasal sinuses. These polyps commonly arise around the ostia of the paranasal sinuses in the middle meatus. Discussion The commonest sites of polyp formation are the ethmoid sinuses and maxillary sinus. Rarely polyps may also arise from the other paranasal sinuses. Sites in the nasal mucosa other than the paranasal sinuses are very rare, though polyps arising from the septum have also been reported. The etiology of nasal polyposis is believed to be due to an inflammatory reaction of the nasal and paranasal sinus mucosa. Conclusion In addition to the theory of altered airway dynamics in the middle meatus, there also appears to be a link between polyp formation and preceding chronic inflammation. This is the most likely explanation for the origin of polyps in unusual sites. We present here a case of a nasal polyp arising from the floor of the nasal cavity. There are no previous records or reports in literature of this unusual site of origin of a nasal polyp.
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Pawliczak, Rafal, Marek L. Kowalski, Marek Danilewicz, Malgorzata Wagrowska-Danilewicz, and Andrzej Lewandowski. "Distribution of Mast Cells and Eosinophils in Nasal Polyps from Atopic and Nonatopic Subjects: A Morphometric Study." American Journal of Rhinology 11, no. 4 (1997): 257–62. http://dx.doi.org/10.2500/105065897781446711.
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The pathogenetic mechanism of nasal polyps remains unknown, although polyps seem to be an expression of chronic nasal inflammation of both allergic and nonallergic origin. The goal of our study was to compare the distribution mast cells and eosinophils (cells traditionally associated with allergic inflammation) in nasal polyps from well defined atopic and nonatopic patients, using advanced morphometric analysis system. Nasal polyps were removed during routine nasal polypectomy performed in 17 atopic and 19 nonatopic patients. Parrafin sections of nasal polyps were stained with haematoxilin/eosin, chromotrope R2 or toluidine blue, and light microscopy, assisted with computerized picture analysis system, was used to count the number of cells in the superficial and stromal layer of the mucosa. Regardless of the presence or absence of atopy, eosinophils were predominant cells in the polyps, and both eosinophils and mast cells were more abundant in the superficial layer than in the stromal layer of the mucosa. The density of eosinophils in both layers and mast cells in the stromal layer was similar in atopic and nonatopic patients. Only the density of mast cells in the superficial layer of the mucosa was slightly higher (p < 0.005 in atopic compared to nonatopic patients). In both groups of patients a significant correlation between the number of mast cells and eosinophils in the superficial layer of the polyp mucosa was found (r = 0.84; p < 0.001). Our study demonstrates that eosinophils and mast cells are abundant in nasal polyps from both atopic and nonatopic patients and that mast cells seem to be more superficially distributed in atopic compared to nonatopic patients.
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Yusran, Yusmawati, and Humairah Medina Liza Lubis. "Epithelial Mucosal Changes and An Inflammation Process of the Cavum Nasi Due to Inhaled Sawdust." Mutiara Medika: Jurnal Kedokteran dan Kesehatan 23, no. 1 (2023): 34–41. http://dx.doi.org/10.18196/mmjkk.v23i1.16623.
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Woodworkers are particularly susceptible to inhalation of sawdust exposure. Exposure to sawdust for a long time causes various health problems and causes the damage of the epithelium to a barrier. This study aims to identify whether inhaled sawdust can cause changes in the nasal mucosa and the occurrence of an inflammatory process. This study was a cross-sectional analytical study. Data were collected from July 2021 to January 2022 from the nasal cavity swab of 35 woodworkers who had worked for 1 to 5 years. The assessment was carried out by cytological examination to identify epithelial changes in the form of mild and moderate dysplasia, while the inflammation was found in the form of acute and chronic inflammation. Twenty-six (74.3%) samples were normal, 7 (20%) samples had mild dysplasia, and 2 (5.7%) samples had moderate dysplasia. Whereas 20 (57.1%) were found to have no inflammation, 8 (22.9%) were with acute inflammation, and 7 (20.0%) were found to have chronic inflammation). Fisher’s exact test showed a relationship between the inflammatory process and epithelial changes (p 0.020). In conclusion, sawdust inhaled showed changes in the epithelial mucosa and inflammatory processes of the nasal cavity.
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Lee, Eun Soo, Woo Yong Bae, Changbae Lee, and Min Gyoung Park. "Delayed Diagnosis Due to Septal Perforation in Patient with Extranodal Natural Killer/T-Cell Lymphoma, Nasal Type." Korean Journal of Otorhinolaryngology-Head and Neck Surgery 63, no. 5 (2020): 223–27. http://dx.doi.org/10.3342/kjorl-hns.2019.00269.
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Extranodal natural killer (NK)/T-cell lymphoma, nasal type is a rare non-Hodgkin lymphoma originating in the nasal cavity or in the paranasal sinuses, and is etiologically closely related with the Epstein Barr Virus infection. It is more commonly found in East Asia, South America, and Mexico than in Europe or North America. Extranodal NK/T-cell lymphoma, nasal type typically shows a crust on the nasal mucosal surface, necrosis, and inflammation. Pathologically, it presents as significant vascular damage and destruction, with apparent tissue necrosis and cytotoxicity. These neoplasms are very aggressive and can show septal perforation, diffuse ulcer lesion on the nasal mucosa, fistula or epistaxis. We experienced a case of the extranodal NK/T-cell lymphoma, nasal type at the nasal septum, which was delayed in diagnosis due to septal perforation, which occurred after septoplasty in a 47-year-old female. Thus, we report this case with a review of literatures.
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Huang, Yu, Zhi-Qiang Guo, Ru-Xin Zhang, et al. "Effect of PM2.5 on MicroRNA Expression and Function in Nasal Mucosa of Rats With Allergic Rhinitis." American Journal of Rhinology & Allergy 34, no. 4 (2020): 543–53. http://dx.doi.org/10.1177/1945892420912367.
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Background Particulate matter 2.5 (PM2.5) refers to particulate matter with aerodynamic equivalent diameter less than or equal to 2.5 µm, which is an important component of air pollution. PM2.5 aggravates allergic rhinitis (AR) and promotes AR nasal mucosa inflammation. Therefore, the influence of PM2.5 inhalation exposure on microRNA (miRNA) expression profiles and function in the nasal mucosa of AR rats was investigated. Methods Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group (ARE group) and AR model PM2.5-unexposed control group (ARC group). The rats of ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days. miRNA expression profiles of the nasal mucosa from both groups were determined using an miRNA gene chip and were verified by quantitative real-time PCR (qRT-PCR). Gene function enrichment analysis was performed using bioinformatics analysis. Results The ARE group revealed 20 significantly differentially expressed miRNAs, including 4 upregulated and 16 downregulated miRNAs (fold change > 1.5 or < 0.66, P < .05). Of these, 9 selected miRNAs were verified by qRT-PCR, and the results of 8 miRNAs were in accordance with the miRNA gene chip results, with highly positive correlation ( r = .8583, P = .0031). Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor β signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways. Conclusions PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an important role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for the prevention and treatment of AR from the effects of environmental pollution on the gene regulation mechanism.
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Gelardi, M., M. L. Fiorella, R. Fiorella, E. Cavallucci, M. Di Gioacchino, and G. Ciprandi. "Lymphocyte Differentiation in the Nasal Mucosa." European Journal of Inflammation 5, no. 3 (2007): 145–50. http://dx.doi.org/10.1177/1721727x0700500305.
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Few cytological studies have investigated the morphologic changes occurring during lymphocyte differentiation in the nose. The aim of the study is to investigate lymphocyte and plasma cell morphology in patients with allergic rhinitis. Nasal cytology was performed in 110 patients (61 men, 49 women) of ages ranging from 12 to 47 years (mean age, 27), 72 of whom were affected by pollen allergic rhinitis (32 allergic to olive, 21 to Parietaria, 13 to grasses, and 6 to cypress) and 38 by perennial allergic rhinitis (allergy to house dust mites). Cytological samples were obtained by scraping with Rhino-Probe™. The samples were collected from the inferior middle turbinate. After fixing and drying, the samples were stained and counted. Cells belonging to the lymphocyte-plasma cell lineage were analyzed. Within this population, 5 different cellular types were identified displaying particular morphologic features of the nucleus and the cytoplasm. These morphological variants constitute various functional stages of B lymphocytes. In allergic inflammation, antigen stimulation induces B lymphocytes to differentiate and become plasma cells. The findings from this strictly morphological study will need to be confirmed by immunohistochemical and immunophenotypic studies.
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Bernstein, Joel M., and William J. Doyle. "Role of Ige-Mediated Hypersensitivity in Otitis Media with Effusion: Pathophysiologic Considerations." Annals of Otology, Rhinology & Laryngology 103, no. 5_suppl (1994): 15–19. http://dx.doi.org/10.1177/00034894941030s505.
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A pathophysiologic model of otitis media with effusion secondary to IgE-mediated hypersensitivity is described. Specific mediators of inflammation are released by mucosal mast cells in the nasal mucosa following the interaction of antigen and specific IgE antibody. These mediators increase vascular permeability, mucosal blood flow, and, most important, mucus production. Furthermore, accessory cell types are recruited by colony-stimulating factors that in turn provide an autocrine-positive feedback for the influx of further inflammatory cells. The eustachian tube is then effectively obstructed by both intrinsic venous engorgement and extrinsic mucus plugs, isolating the middle ear space from the ambient environment The net result is the increased exchange of nitrogen into the middle ear mucosa from the middle ear cavity. This causes the development of a significant middle ear underpressure that disrupts tight junctions and allows for transudation of fluids into the middle ear space. The prolonged obstruction of the eustachian tube with mucus results in middle ear inflammation, mucosal metaplasia, and increased glandular activities, all of which are hallmarks of chronic otitis media with effusion.
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Miljkovic, Dijana, Alkis Psaltis, Peter-John Wormald, and Sarah Vreugde. "Naive and Effector B-cell Subtypes are Increased in Chronic Rhinosinusitis with Polyps." American Journal of Rhinology & Allergy 32, no. 1 (2018): 3–6. http://dx.doi.org/10.2500/ajra.2018.32.4496.
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Background Recent studies demonstrated that B cells and their chemoattractants are elevated in the nasal mucosa of patients with chronic rhinosinusitis (CRS) with nasal polyposis (CRSwNP). However, the presence of naive B cells and of plasmablasts and memory B-cell subsets in the mucosa and periphery of the same patient with CRS is yet to be characterized. Objective Here we sought to quantify naive, plasmablasts, and memory B cells in mucosal tissue and peripheral blood of patients with CRSwNP, patients with CRS without nasal polyps (CRSsNP), and control patients. Methods Polyps, mucosa, and peripheral blood samples were prospectively collected from the patients with CRS and from the non-CRS controls. We used flow cytometry to distinguish among naive, plasmablast, and memory B cells in sinus tissue and peripheral blood. Results A total of 45 patients were recruited for the study. The patients with CRSwNP had significantly increased mucosal B-cell numbers versus the controls (3.39 ± 4.05% versus 0.39 ± 1.05% of live cells; p < 0.01, Kruskal-Wallis test), which included naive B cells (0.61 ± 0.94 versus 0.11 ± 0.24% of live cells; p < 0.03, Kruskal-Wallis test), plasmablasts (0.06 ± 0.26 versus 0.00 ± 0.00% e cells; p < 0.055, Kruskal-Wallis test), and memory B cells (0.62 ± 1.26 versus 0.05 ± 0.15% of live cells; p < 0.02, Kruskal-Wallis test). Conclusion Our study identified increased frequencies of different B-cell subtypes in the mucosa of patients with CRSwNP but not in the peripheral blood. We also found that patients with CRSwNP had significantly increased B-cell subtypes compared with the patients with CRSsNP and the controls. These results implied a potential role for mucosal B cells in the ongoing inflammation in patients with CRSwNP.
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Xiao, Lifeng, Li Jiang, Qi Hu, and Yuru Li. "MicroRNA-133b Ameliorates Allergic Inflammation and Symptom in Murine Model of Allergic Rhinitis by Targeting Nlrp3." Cellular Physiology and Biochemistry 42, no. 3 (2017): 901–12. http://dx.doi.org/10.1159/000478645.
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Background: Emerging evidences indicate that post-transcriptional regulation by microRNAs is critical in allergic rhinitis (AR) pathogenesis. MircroRNA-133b (miR-133b) was recently suggested as a potential predictor of AR. However, the in vivo effect of miR-133b on AR is unclear. Methods: AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). MiR-133b agomir was then intranasally administrated to mice after OVA challenge for another 7 days. The symptom of nasal rubbing and sneezing were recorded after the last OVA challenge. Nasal mucosa tissues and serum were collected. MiR-133b expression, serum OVA-specific immunoglobulin E (IgE) concentration, proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-10 and IFN-γ) levels, and Nlrp3 inflammasome activation were measured by RT-PCR, ELISA, western blotting or immunohistochemistry, respectively. Histopathologic changes were evaluated using hematoxylin and eosin and Sirius red staining. The luciferase activity and protein expression of Nlrp3 were also determined. Results: MiR-133b expression was significantly decreased in nasal mucosa of AR mice, which was restored by nasal administration with miR-133b agomir. Upregulation of miR-133b markedly reduced the concentration of OVA-specific IgE, the frequencies of nasal rubbing and sneezing, and the levels of cytokines (TNF-α, IL-4, IL-5 and IFN-γ). Levels of IL-4, IL-5, IL-10 and IFN-γ produced by cervical lymph node cells were significantly lowered in miR-133b agomir-treated mice. Moreover, miR-133b also appeared to strongly attenuate pathological alterations and eosinophils and mast cells infiltration in nasal mucosa. Notably, we demonstrated for the first time that miR-133b negatively regulated Nlrp3 expression through binding with the 3’ untranslated region of Nlrp3. Consequently, infection of miR-133b in nasal mucosa remarkably suppressed the Nlrp3 inflammasome activation, as evidenced by reduced Nlrp3, Caspase-1, ASC, IL-18 and IL-1 expressions. Conclusion: MiR-133b alleviates allergic symptom in AR mice by inhibition of Nlrp3 inflammasome-meditated inflammation. These findings provide us an insight into the potential role of miR-133b in relation to AR treatment.
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Shrivastava, Ravi. "An Instant, Safe, Antihistamine, Anti-Inflammatory and Decongestant Polymeric Nasal Barrier to Prevent and To Treat Allergic Rhinitis in Children." Journal of Clinical Research and Reports 7, no. 5 (2021): 01–09. http://dx.doi.org/10.31579/2690-1919/164.
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Introduction: Allergic rhinitis (AR) in children is a common chronic pathology with a strong impact on patient quality of life. The main physiopathology affects the nasal cavity as a multi-factorial disease involving nasal mucosa damage, nasal inflammation with high concentrations of histamine, pro-inflammatory cytokines such as histamine, TNF-α, IL-4, IL-5, IL-6, IL-10, IL-13, and IgE antibodies on the nasal mucosa. Systemic entry of these proteins through damaged nasal mucosa maintains continued inflammatory and allergen cascades. Therefore, an ideal treatment should be multitarget in order to stop allergen exposure, inflammation, and nasal mucosa barrier degradation, but such treatments are nearly impossible to conceive. We envisaged an osmotic and protective nasal barrier film, not only capable of protecting the nasal mucosa from allergen exposure but also of trapping and neutralizing selected cytokines and cleaning the nasal surface continuously without using any harmful substance for children. Materials and Methods: We associated highly osmotic glycerol solution with specific plant polymers to conceive an osmotic but stable film. As plant polymers (tannins) can bind with selective proteins, a range of glycerol binding non-cytotoxic polymers were screened using the sandwich ELISA method to select those having binding affinity for allergen induced nasal proinflammatory cytokines. After verifying cytotoxicity and irritant potential, a 15-day observational clinical study was performed with approval from the ethics committee on 30 children aged between 4-13, suffering from allergic rhinitis. The test product (TP) was supplied in 15-ml nasal sprays and applied 2-3 times per day for a period of 15 days. Saline solution served as control (CP). The scores of nasal and ocular symptoms, effect on quality of life, eosinophil count in nasal smears, and need for antihistamine treatment was evaluated at the start, at 30 minutes and on days 2, 3 and 15 of treatment. Results: A few specific polymers were able to bind with selected cytokines and histamine at adequate filmogen concentrations. The osmotic film was stable, non-irritant and was able to clean the nasal mucosa continuously for 4-6h after each application. Clinical observations of Total Nasal Symptom Score (TNSS) grouping the scores of nasal congestion, runny nose, sneezing, and itching, revealed a strong decrease right after the 1st treatment in both groups but the reduction was much stronger and faster with the TP. The mean TNSS score reduction was 44.74% in CP vs 83.53% in the TP group after 7 days of treatment (p<0.001). Total Ocular Symptom Score (TOSS) was decreased by 21.13% and 51.41% in CP v/s 35.12 and 99.59% in TP group on days 2 and 7, respectively. Nasal smear eosinophil count was equally strongly reduced in the TP v/s CP group. No treatment-related side effects were recorded in any of the groups. Conclusion: Protecting the nasal mucosa against allergens, neutralizing inflammatory cytokines, and keeping the nasal surface clean with an osmotic polymeric film, constitute a major breakthrough for the treatment of allergic rhinitis in children. This simple but scientific and logical approach should avoid exposing children to chemicals and to their long-term side effects.