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Journal articles on the topic 'Peritonitis model in mice'

Author: Grafiati

Published: 5 June 2025

Last updated: 2 August 2025

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1

Goswami, Manish, Deepak Sharma, Nazir M. Khan, Rahul Checker, Santosh Kumar Sandur, and Narendra Jawali. "Antioxidant supplementation enhances bacterial peritonitis in mice by inhibiting phagocytosis." Journal of Medical Microbiology 63, no. 3 (2014): 355–66. http://dx.doi.org/10.1099/jmm.0.067173-0.

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Antioxidants are known to exhibit numerous health benefits including anti-ageing, anti-apoptotic and immuno-stimulatory effects. However, we present the data showing counterproductive effects of therapeutically relevant antioxidants on bacterial clearance by the immune system in a murine peritonitic model. The antioxidants ascorbic acid, glutathione and N-acetylcysteine augmented morbidity and mortality in mice carrying Eshcerichia coli-induced acute bacterial peritonitis. Treatment of peritonitic mice with antioxidants significantly increased their bacterial load in the range of 0.3–2 logs. A

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Ishii, Yasuo, Tokihiko Sawada, Akira Shimizu, et al. "An experimental sclerosing encapsulating peritonitis model in mice." Nephrology Dialysis Transplantation 16, no. 6 (2001): 1262–66. http://dx.doi.org/10.1093/ndt/16.6.1262.

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Clark, Jessica A., Heng Gan, Alexandr J. Samocha, Amy C. Fox, Timothy G. Buchman, and Craig M. Coopersmith. "Enterocyte-specific epidermal growth factor prevents barrier dysfunction and improves mortality in murine peritonitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 3 (2009): G471—G479. http://dx.doi.org/10.1152/ajpgi.00012.2009.

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Systemic administration of epidermal growth factor (EGF) decreases mortality in a murine model of septic peritonitis. Although EGF can have direct healing effects on the intestinal mucosa, it is unknown whether the benefits of systemic EGF in peritonitis are mediated through the intestine. Here, we demonstrate that enterocyte-specific overexpression of EGF is sufficient to prevent intestinal barrier dysfunction and improve survival in peritonitis. Transgenic FVB/N mice that overexpress EGF exclusively in enterocytes ( IFABP-EGF) and wild-type (WT) mice were subjected to either sham laparotomy

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Ni, Jie, Yvette Cnops, Rachel M. McLoughlin, Nicholas Topley, and Olivier Devuyst. "Inhibition of Nitric Oxide Synthase Reverses Permeability Changes in a Mouse Model of Acute Peritonitis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 25, no. 3_suppl (2005): 11–14. http://dx.doi.org/10.1177/089686080502503s03.

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Acute peritonitis is the most frequent complication of peritoneal dialysis. Previous studies have suggested a major role for nitric oxide (NO) in the permeability changes and loss of ultrafiltration induced by acute peritonitis. In this study, we further investigated the potential role of NO in a mouse model of peritonitis induced by Escherichia coli lipopolysaccharide (LPS). A 2-hour peritoneal equilibration test was performed in control and LPS-treated mice using 7% glucose dialysate supplemented or not with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The levels of N

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Liu, Shaoguang, Shaotong Zhang, Yulong Sun, and Wence Zhou. "Transcriptomics Changes in the Peritoneum of Mice with Lipopolysaccharide-Induced Peritonitis." International Journal of Molecular Sciences 22, no. 23 (2021): 13008. http://dx.doi.org/10.3390/ijms222313008.

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Peritonitis caused by LPS is a severe clinical challenge, which causes organ damage and death. However, the mechanism of LPS-induced peritonitis has not been fully revealed yet. Here, we investigated the transcriptome profile of the peritoneal tissue of LPS-induced peritonitis in mice. A model of LPS-induced peritonitis in mice was established (LPS 10 mg/kg, i.p.), and the influence of TAK 242 (TLR4 inhibitor) on the level of inflammatory cytokines in mouse peritoneal lavage fluid was investigated by using an ELISA test. Next, the peritoneal tissues of the three groups of mice (Control, LPS, a

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Steinhauser, Matthew L., Cory M. Hogaboam, Nickolas W. Lukacs, Robert M. Strieter, and Steven L. Kunkel. "Multiple Roles for IL-12 in a Model of Acute Septic Peritonitis." Journal of Immunology 162, no. 9 (1999): 5437–43. http://dx.doi.org/10.4049/jimmunol.162.9.5437.

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Abstract The present study addressed the role of IL-12 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Although CLP surgery induced IL-12 production at 6 and 24 h after surgery, IL-12 immunoneutralization was clearly deleterious in this model: 54% of CLP mice receiving preimmune serum survived, whereas mice administered IL-12 antisera prior to CLP experienced a 25% survival rate. IL-12 immunoneutralization not only led to increased mortality, but also appeared to promote a shift away from IL-12 and IFN-γ, in favor of IL-10. This cytokine shift corresponde

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Lan, Jing, Hong Zhang, Hui Zhao, et al. "Cord Blood Natural Killer Cells Inhibit Sepsis Caused by Feces-Induced Acute Peritonitis via Increasing Endothelium Integrity." Cell Transplantation 31 (January 2022): 096368972210902. http://dx.doi.org/10.1177/09636897221090257.

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Sepsis is associated with acute peritonitis, which can be induced by lipopolysaccharide exposure and feces. Generally, lipopolysaccharide induces mono-microbial peritonitis, whereas feces cause poly-microbial peritonitis; the latter is a more complicated and closer to the clinical diseases. Although several reports have discussed the mechanism of immune response in peritonitis-induced sepsis, however, the role of natural killer (NK) cells in sepsis, especially the relationship between NK cells and stabilization of the vascular endothelial barrier, is still unclear. Accordingly, in this study,

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Kang, Xu-Qi, Yue Qiao, Xiao-Yang Lu, et al. "Tocopherol polyethylene glycol succinate-modified hollow silver nanoparticles for combating bacteria-resistance." Biomaterials Science 7, no. 6 (2019): 2520–32. http://dx.doi.org/10.1039/c9bm00343f.

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Diedrich, Stephan, Julia van der Linde, Michael Nielson, et al. "The MRI Sepsis Score: An Innovative Tool for the Evaluation of Septic Peritonitis in Mice Using 7-Tesla Small Animal MRI." European Surgical Research 59, no. 3-4 (2018): 126–42. http://dx.doi.org/10.1159/000490663.

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Background: Magnetic resonance imaging (MRI) techniques are rarely used in the context of abdominal sepsis and in sepsis research. This study investigates the impact of MRI for monitoring septic peritonitis in an animal model (colon ascendens stent-induced peritonitis, CASP). The CASP model closely mimics that of human disease and is highly standardized. The most frequently employed readout parameter in mouse CASP studies is prolonged or decreased rate of survival. Monitoring the progression of peritonitis via MRI could provide a helpful tool in the evaluation of severity. The use of alternati

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Woods, Dustin R., Susan Heffley, James C. Peyton, and William G. Cheadle. "Antibiotic Modulation in a Clinically Relevant Model of Chronic Intraabdominal Infection." American Surgeon 72, no. 7 (2006): 655–60. http://dx.doi.org/10.1177/000313480607200717.

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Continuous and twice-daily cefoxitin dosing was used in a highly lethal model of acute peritonitis in mice using intraperitoneal (IP) Klebsiella pneumoniae (Kpn). The purpose was to use antibiotics to create a model of chronic infection. Male Balb/c mice (averaging 20 g body weight) were inoculated IP with 103 colony-forming units (CFU) Kpn serotype 2. Controls received subcutaneous saline either twice daily or continuously. Antibiotic groups received 300 mg/kg per day of cefoxitin either twice daily or continuously. Survival and daily weight losses were determined. Another group was inoculate

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Zantl, N., C.-D. Heidecke, B. Holzmann, and K. Pfeffer. "COLON ASCENDENS STENT PERITONITIS: A NOVEL SURGICAL MODEL FOR THE INDUCTION OF BACTERIAL PERITONITIS/SEPSIS IN MICE." Shock 7, Supplement (1997): 137. http://dx.doi.org/10.1097/00024382-199703001-00556.

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Echtenacher, Bernd, Marina A. Freudenberg, Robert S. Jack, and Daniela N. Männel. "Differences in Innate Defense Mechanisms in Endotoxemia and Polymicrobial Septic Peritonitis." Infection and Immunity 69, no. 12 (2001): 7271–76. http://dx.doi.org/10.1128/iai.69.12.7172-7276.2001.

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ABSTRACT Loss, reduction, or enhancement of the ability to respond to bacterial lipopolysaccharide (LPS) has no influence on survival of mice in a model of postoperative polymicrobial septic peritonitis induced by cecal ligation and puncture (CLP). This was demonstrated by using either mice with a defective Tlr4 gene, which encodes the critical receptor molecule for LPS responses, or mice deficient for LPS binding protein (LBP) or mice sensitized to LPS byPropionibacterium acnes. Though interleukin-12 (IL-12) and gamma interferon (IFN-γ) play an important role in the sensitivity to LPS as well

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Cao, Shirong, Shu Li, Yating Wang, et al. "Acetylation of HMGB1 by JNK1 Signaling Promotes LPS-Induced Peritoneal Mesothelial Cells Apoptosis." BioMed Research International 2018 (November 12, 2018): 1–12. http://dx.doi.org/10.1155/2018/2649585.

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Increased high mobility group box 1 (HMGB1) in dialysis effluence is associated with the presence of peritoneal dialysis-related peritonitis in patients and peritoneal dysfunction in acute peritonitis mice model, but it remains unclear whether HMGB1 is involved in peritoneal mesothelial cell injury and functions via molecular posttranslational modifications by acetylation in this process. Here we first showed correlation between HMGB1 acetylation level in dialysis effluence of patients and occurrence of Gram-negative peritonitis. The increased level of acetylated HMGB1 was similarly observed u

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Huang, Miao-Tzu, Karen Y. Larbi, Christoph Scheiermann, et al. "ICAM-2 mediates neutrophil transmigration in vivo: evidence for stimulus specificity and a role in PECAM-1–independent transmigration." Blood 107, no. 12 (2006): 4721–27. http://dx.doi.org/10.1182/blood-2005-11-4683.

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AbstractICAM-2 has been implicated in leukocyte transmigration in vitro, but there is little in vivo evidence to support this. To address this, neutrophil migration was investigated in ICAM-2–deficient mice (KO) and in wild-type (WT) mice treated with an anti–ICAM-2 blocking monoclonal antibody (mAb) (3C4). In a peritonitis model, IL-1β–induced accumulation of neutrophils was significantly reduced in mice treated with 3C4 (51% inhibition) and in KO mice (41% inhibition). In contrast, TNF-α– or thioglycolate-induced responses were not suppressed in KO mice. Analysis of IL-1β–induced leukocyte r

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Parameswaran, Narayanan, Babu Gonipeta, Sitaram Parvataneni, Nandakumar Packiriswamy та Deepika Sharma. "β-arrestin-1 negatively regulates inflammatory response to polymicrobial sepsis in mice (110.11)". Journal of Immunology 186, № 1_Supplement (2011): 110.11. http://dx.doi.org/10.4049/jimmunol.186.supp.110.11.

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Abstract β-arrestins are scaffolding proteins that regulate a number of receptor signaling pathways including Toll-like receptors. We recently demonstrated that mice lacking either β-arrestin-1 or β-arrestin-2 are protected from lipopolysaccharide-induced lethality and have a markedly reduced inflammatory response. To assess the role of β-arrestin-1 in a clinically relevant model of sepsis, we subjected wild type and β-arrestin-1 knockout mice to cecal-ligation and puncture (CLP) to mimick septic peritonitis and polymicrobial sepsis. Surprisingly, we found that, mortality of β-arrestin-1 knock

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Shi, Zheng-Zheng, Bing Han, Geetha M. Habib, Martin M. Matzuk та Michael W. Lieberman. "Disruption of γ-Glutamyl Leukotrienase Results in Disruption of Leukotriene D4 Synthesis In Vivo and Attenuation of the Acute Inflammatory Response". Molecular and Cellular Biology 21, № 16 (2001): 5389–95. http://dx.doi.org/10.1128/mcb.21.16.5389-5395.2001.

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ABSTRACT To study the function of γ-glutamyl leukotrienase (GGL), a newly identified member of the γ-glutamyl transpeptidase (GGT) family, we generated null mutations in GGL (GGLtm1) and in both GGL and GGT (GGLtm1-GGTtm1) by a serial targeting strategy using embryonic stem cells. Mice homozygous for GGLtm1 show no obvious phenotypic changes. Mice deficient in both GGT and GGL have a phenotype similar to the GGT-deficient mice, but ∼70% of these mice die before 4 weeks of age, at least 2 months earlier than mice deficient only in GGT. These double-mutant mice are unable to cleave leukotriene C

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Hogaboam, Cory M., Matthew L. Steinhauser, Harold Schock, et al. "Therapeutic Effects of Nitric Oxide Inhibition during Experimental Fecal Peritonitis: Role of Interleukin-10 and Monocyte Chemoattractant Protein 1." Infection and Immunity 66, no. 2 (1998): 650–55. http://dx.doi.org/10.1128/iai.66.2.650-655.1998.

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ABSTRACT This study demonstrates that the therapeutic effect of a nitric oxide inhibitor in a murine model of fecal peritonitis is mediated in part by increased levels of interleukin-10 (IL-10) and monocyte chemoattractant protein 1 (MCP-1). Female CD1 mice were subjected to cecal ligation and puncture (CLP) with a 21-gauge needle and, immediately following surgery, were injected intraperitoneally with saline,N G-nitro-l-arginine methyl ester (l-NAME; 8 mg/kg), orN G-nitro-d-arginine methyl ester (d-NAME; 8 mg/kg). At 96 h after surgery and drug treatment, 20% of mice that received d-NAME had

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Dou, Jiangli, Qingsong Xu, Chengyu Tan, et al. "Effects of chitosan oligosaccharides on neutrophils from glycogen-induced peritonitis mice model." Carbohydrate Polymers 75, no. 1 (2009): 119–24. http://dx.doi.org/10.1016/j.carbpol.2008.07.005.

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da Silva, Morgana Duarte, Giselle Guginski, Maria Fernanda de Paula Werner, Cristiane Hatsuko Baggio, Rodrigo Marcon, and Adair Roberto Soares Santos. "Involvement of Interleukin-10 in the Anti-Inflammatory Effect of Sanyinjiao (SP6) Acupuncture in a Mouse Model of Peritonitis." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–9. http://dx.doi.org/10.1093/ecam/neq036.

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In this study, we determined the anti-inflammatory effect of manual acupuncture at the Sanyinjiao or Spleen 6 (SP6) point on carrageenan-induced peritonitis in mice and investigated mechanisms that may underlie this effect. In the first set of experiments, male Swiss mice were allocated into five groups: the control (sterile saline), dexamethasone (DEXA), invasive sham-acupuncture (non-acupoint), SP6 acupuncture and carrageenan-treated groups. Ten minutes after needle retention or 30 min after DEXA treatment, mice received an intraperitoneal injection of carrageenan (750 μg/mouse). After 4 h,

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Lucena, Alessandra, Cássio Souza, Jéssica Jales, et al. "The Bisindole Alkaloid Caulerpin, from Seaweeds of the Genus Caulerpa, Attenuated Colon Damage in Murine Colitis Model." Marine Drugs 16, no. 9 (2018): 318. http://dx.doi.org/10.3390/md16090318.

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Caulerpin (CLP), an alkaloid from algae of the genus Caulerpa, has shown anti-inflammatory activity. Therefore, this study aimed to analyze the effect of CLP in the murine model of peritonitis and ulcerative colitis. Firstly, the mice were submitted to peritonitis to evaluate which dose of CLP (40, 4, or 0.4 mg/kg) could decrease the inflammatory infiltration in the peritoneum. The most effective doses were 40 and 4 mg/kg. Then, C57BL/6 mice were submitted to colitis development with 3% dextran sulfate sodium (DSS) and treated with CLP at doses of 40 and 4 mg/kg. The disease development was an

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Pagano, Rosana L., Mario Mariano, and Renata Giorgi. "Neutrophilic Cell-Free Exudate Induces Antinociception Mediate by the Protein S100A9." Mediators of Inflammation 2006 (2006): 1–6. http://dx.doi.org/10.1155/mi/2006/36765.

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Calcium-binding protein S100A9 (MRP-14) induces antinociceptive effect in an experimental model of painful sensibility and participates of antinociception observed during neutrophilic peritonitis induced by glycogen or carrageenan in mice. In this study, the direct antinociceptive role of the protein S100A9 in neutrophilic cell-free exudates obtained of mice injected with glycogen was investigated. Mice were intraperitoneally injected with a glycogen solution, and after4,8,24, and48hours, either the pattern of cell migration of the peritoneal exudate or the nociceptive response of animals was

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Fernandez-Boyanapalli, Ruby, S. Courtney Frasch, David W. H. Riches, R. William Vandivier, Peter M. Henson та Donna L. Bratton. "PPARγ activation normalizes resolution of acute sterile inflammation in murine chronic granulomatous disease". Blood 116, № 22 (2010): 4512–22. http://dx.doi.org/10.1182/blood-2010-02-272005.

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Absence of a functional nicotinamide adenine dinucleotide phosphate (NADPH) oxidase predisposes chronic granulomatous disease (CGD) patients to infection, and also to unexplained, exaggerated inflammation. The impaired recognition and removal (efferocytosis) of apoptotic neutrophils by CGD macrophages may contribute to this effect. We hypothesized that peroxisome proliferator-activated receptor γ (PPARγ) activation during CGD inflammation is deficient, leading to altered macrophage programming and decreased efferocytosis, and that PPARγ agonism would enhance resolution. using the gp91phox−/− m

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Massa, Christine, Emma Braine, Jason Lenzo, et al. "The effect of tissue type-plasminogen activator deletion and associated fibrin(ogen) deposition on macrophage localization in peritoneal inflammation." Thrombosis and Haemostasis 95, no. 04 (2006): 659–67. http://dx.doi.org/10.1160/th05-06-0405.

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SummaryThere are two plasminogen activators (PAs), urokinase type-PA (u-PA) and tissue type-PA (t-PA). While u-PA is considered to be involved in cellular migration and tissue remodeling and t-PA in fibrinolysis, this distinction is not always clear-cut. With the use of u-PA and t-PA gene deficient mice (u-PA-/and t-PA-/mice, respectively) we have assessed the role of each PA in acute peritonitis. The cellular infiltrate in both thioglycolateand antigen-induced peritoneal exudates was unaffected in u-PA-/mice; in contrast, in t-PA-/mice, the macrophage numbers, particularly of the Mac-1hi popu

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Chan, Goldia, Christopher Fry, and Jean Nemzek. "Impact of thermoneutral acclimation on a murine model of polymicrobial peritonitis." PLOS One 20, no. 5 (2025): e0322855. https://doi.org/10.1371/journal.pone.0322855.

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To examine the effects of ambient temperature on the reproducibility and translation of a murine sepsis model, we hypothesized that acclimation of mice in temperatures within their thermoneutral zone would alter immune responses and outcomes compared to standard housing temperatures. Mice housed for one week in thermoneutral (30°C) as compared to standard (22°C) conditions displayed lower counts of circulating neutrophils (0.52 ± 0.20 vs. 1.10 ± 0.54 x103/μL; p = 0.011) and peritoneal macrophages (0.80 ± 0.57 vs. 1.62 ± 0.62 x 105/μL; p = 0.002) as well as reduced in vitro production of IFN-γ

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Rodgers, Kathleen, Shiquan Xiong, Theresa Espinoza, Norma Roda, Sonia Maldonado, and Gere S. diZerega. "Angiotensin II Increases Host Resistance to Peritonitis." Clinical Diagnostic Laboratory Immunology 7, no. 4 (2000): 635–40. http://dx.doi.org/10.1128/cdli.7.4.635-640.2000.

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ABSTRACT Studies by other laboratories have shown that angiotensin II (AII) can affect the function of cells which comprise the immune system. In the present study, the effect of AII on the function of peritoneal macrophages and peripheral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentage of cells that phagocytosed opsonized yeast and the number of yeast per macrophage. Furthermore, AII increased the respiratory burst capacity of peritoneal macrophages from mice and rats and peripheral blood mononuc

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Larmann, Jan, Tim Frenzel, Anke Hahnenkamp, et al. "In Vivo Fluorescence-mediated Tomography for Quantification of Urokinase Receptor-dependent Leukocyte Trafficking in Inflammation." Anesthesiology 113, no. 3 (2010): 610–18. http://dx.doi.org/10.1097/aln.0b013e3181e99bfc.

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Background Inflammation is characterized by leukocyte recruitment. Macrophages and neutrophils contribute to tissue damage and organ dysfunction. Modulating leukocyte invasion can protect from these adverse effects. Leukocyte recruitment critically depends on the urokinase-type plasminogen activator receptor (u-PAR). We here use a novel technique to longitudinally quantify cell trafficking in inflammatory models in live animals. Methods Near-infrared fluorophore-labeled leukocytes were adoptively transferred to mice with thioglycollate peritonitis to study leukocyte trafficking to sites of inf

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Huang, Yuqing, Yi Ning, Zhiwei Chen, et al. "A Novel IRAK4 Inhibitor DW18134 Ameliorates Peritonitis and Inflammatory Bowel Disease." Molecules 29, no. 8 (2024): 1803. http://dx.doi.org/10.3390/molecules29081803.

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IRAK4 is a critical mediator in NF-κB-regulated inflammatory signaling and has emerged as a promising therapeutic target for the treatment of autoimmune diseases; however, none of its inhibitors have received FDA approval. In this study, we identified a novel small-molecule IRAK4 kinase inhibitor, DW18134, with an IC50 value of 11.2 nM. DW18134 dose-dependently inhibited the phosphorylation of IRAK4 and IKK in primary peritoneal macrophages and RAW264.7 cells, inhibiting the secretion of TNF-α and IL-6 in both cell lines. The in vivo study demonstrated the efficacy of DW18134, significantly at

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Steinhauser, M. L., C. M. Hogaboam, A. Matsukawa, N. W. Lukacs, R. M. Strieter, and S. L. Kunkel. "Chemokine C10 Promotes Disease Resolution and Survival in an Experimental Model of Bacterial Sepsis." Infection and Immunity 68, no. 11 (2000): 6108–14. http://dx.doi.org/10.1128/iai.68.11.6108-6114.2000.

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ABSTRACT Previous studies have suggested that the C-C chemokine C10 is involved in the chronic stages of host defense reactions. The present study addressed the role of C10 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Unlike other C-C chemokines, C10 levels in the peritoneal wash were increased approximately 30-fold above baseline levels at 48 h after CLP surgery. Immunoneutralization of peritoneal C10 levels with polyclonal anti-C10 antiserum during CLP-induced peritonitis negatively impacted mouse survival over 4 days. In contrast, when 500 ng of rec

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Wellmer, Andreas, Joachim Gerber, Jasmin Ragheb, et al. "Effect of Deficiency of Tumor Necrosis Factor Alpha or Both of Its Receptors on Streptococcus pneumoniae Central Nervous System Infection and Peritonitis." Infection and Immunity 69, no. 11 (2001): 6881–86. http://dx.doi.org/10.1128/iai.69.11.6881-6886.2001.

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ABSTRACT Tumor necrosis factor alpha (TNF-α) and TNF-β are key mediators in bacterial inflammation. We therefore examined the role of TNF-α and its two receptors in murine pneumococcal central nervous system infection. TNF-α knockout mice and age- and sex-matched controls and TNF receptor (p55 and p75)-deficient mice and heterozygous littermates were infected intracerebrally with a Streptococcus pneumoniae type 3 strain. Mice were monitored until death or were killed 36 h after infection. Bacterial titers in blood, spleen, and brain homogenates were determined. Leukocyte infiltration and neuro

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Stolarski, Allan E., Jiann-Jyh Lai, Jiyoun Kim, Kenneth L. Rock, and Daniel Remick. "GENETIC ABLATION OF THE C-TYPE LECTIN RECEPTOR CLEC2D INCREASES PERITONITIS MORTALITY, INFLAMMATION, AND PHYSIOLOGY WITHOUT DIMINISHING ORGAN INJURY." Shock 62, no. 3 (2024): 437–46. http://dx.doi.org/10.1097/shk.0000000000002413.

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ABSTRACT Background: Sepsis accounts for substantial morbidity and mortality motivating investigators to continue the search for pathways and molecules driving the pathogenesis of the disease. The current study examined if the novel C-type lectin receptor (CLR), Clec2d, plays a significant role in the pathogenesis of sepsis. Methods: Clec2d knockout (KO) mice were fully backcrossed onto the C57/BL6 background. Acute endotoxemia was induced with an intraperitoneal injection of lipopolysaccharide (LPS). Sepsis was induced in two different models, cecal ligation and puncture (CLP) and Pseudomonas

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An, Xiaoyu, Kaixia Lian, Jia Zheng, Fei Jian, Henry Li та Tao Yang. "724 Evaluation of an anti-human IL-1β antibody in monosodium urate crystals-induced peritonitis model in hIL-1β HuGEMM™ mice". Journal for ImmunoTherapy of Cancer 9, Suppl 2 (2021): A753. http://dx.doi.org/10.1136/jitc-2021-sitc2021.724.

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BackgroundGout is a chronic inflammatory disease featuring the deposition of monosodium urate (MSU) crystals in the synovial fluid of patients, followed by NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammasome activation and bioactive IL-1β release, which recruits neutrophils to the local inflammation sites. Blocking IL-1β function is becoming a a potent therapeutic approach for gout and gouty arthritis. Conventional MSU-induced peritonitis in C57BL/6 mice provides a simple and rapid evaluation of therapeutics targeting inflammasome activation. However, this murine model has li

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Zasłona, Zbigniew, Carlos H. Serezani, Katsuhide Okunishi, David M. Aronoff, and Marc Peters-Golden. "Prostaglandin E2 restrains macrophage maturation via E prostanoid receptor 2/protein kinase A signaling." Blood 119, no. 10 (2012): 2358–67. http://dx.doi.org/10.1182/blood-2011-08-374207.

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Abstract Prostaglandin E2 (PGE2) is a lipid mediator that acts by ligating 4 distinct G protein–coupled receptors, E prostanoid (EP) 1 to 4. Previous studies identified the importance of PGE2 in regulating macrophage functions, but little is known about its effect on macrophage maturation. Macrophage maturation was studied in vitro in bone marrow cell cultures, and in vivo in a model of peritonitis. EP2 was the most abundant PGE2 receptor expressed by bone marrow cells, and its expression further increased during macrophage maturation. EP2-deficient (EP2−/−) macrophages exhibited enhanced in v

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Khadagwanshi, Dipika, Sonkia Trivedi, Preeti Patel, and Megha Jha. "Effect of Phaseolus vulgaris on E. coli induced peritonitis and bacteraemia in mice." Journal of Drug Delivery and Therapeutics 9, no. 4-s (2019): 310–14. http://dx.doi.org/10.22270/jddt.v9i4-s.3323.

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Infectious or non-infectious peritonitis leads to systemic inflammation due to violation of the peritoneum which is often fatal. Evidences suggest that common bean (Phaseolus vulgaris L.) is a source of nutrients and contains phenolic compounds having antioxidant activity and its consumption has been linked with improved health benefits. The aim of the present investigation was evaluate the in vitro antibacterial, antioxidant activity and protective potential of the methanolic extract of P. vulgaris in E. coli induced model of peritonitis in albino wistar rats. Rats were pre-treated with 200 m

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Verma, Taru, Shamik Majumdar, Shikha Yadav, Syed Moiz Ahmed, Siva Umapathy, and Dipankar Nandi. "Cell-free hemoglobin is a marker of systemic inflammation in mouse models of sepsis: a Raman spectroscopic study." Analyst 146, no. 12 (2021): 4022–32. http://dx.doi.org/10.1039/d1an00066g.

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Dupont, Herve, Philippe Montravers, Jacqueline Mohler, and Claude Carbon. "Disparate Findings on the Role of Virulence Factors of Enterococcus faecalis in Mouse and Rat Models of Peritonitis." Infection and Immunity 66, no. 6 (1998): 2570–75. http://dx.doi.org/10.1128/iai.66.6.2570-2575.1998.

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ABSTRACT The role of Enterococcus faecalis in polymicrobial peritonitis is still debated. Virulence factors expressed in some enterococcal strains might be involved in the pathogenicity of these organisms. To clarify their role, three of these virulence factors (cytolysin, gelatinase, and aggregation substance) were studied in six isogenic strains of E. faecalis expressing various combinations of these factors. Since the pathogenic effects of enterococci are only moderate, the expression of their virulence might vary from one animal species to another and from one type of infection to another.

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Weber, Georg F., Sylvia Schlautkötter, Simone Kaiser-Moore, Felicitas Altmayr, Bernhard Holzmann, and Heike Weighardt. "Inhibition of Interleukin-22 Attenuates Bacterial Load and Organ Failure during Acute Polymicrobial Sepsis." Infection and Immunity 75, no. 4 (2007): 1690–97. http://dx.doi.org/10.1128/iai.01564-06.

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ABSTRACT Interleukin-22 (IL-22) is a recently discovered proinflammatory cytokine, structurally related to IL-10. Since IL-22 is induced by lipopolysaccharide in vivo, we studied the role of IL-22 in a model of polymicrobial peritonitis. Quantitative real-time reverse transcription-PCR analysis showed marked induction of IL-22 and IL-22 receptor in spleen and kidney during the course of sepsis. The biological activity of IL-22 is modulated by IL-22-binding protein (IL-22BP), which is considered a natural antagonist of IL-22. To further analyze the role of IL-22 during septic peritonitis, mice

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Ren, Yunjia, Li Hua, Xiuping Meng, et al. "Correlation of Surface Toll-Like Receptor 9 Expression with IL-17 Production in Neutrophils during Septic Peritonitis in Mice Induced byE. coli." Mediators of Inflammation 2016 (2016): 1–17. http://dx.doi.org/10.1155/2016/3296307.

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IL-17 is a proinflammatory cytokine produced by various immune cells. Polymorphonuclear neutrophils (PMNs) are the first line of defense in bacterial infection and express surface Toll-like receptor 9 (sTLR9). To study the relationship of sTLR9 and IL-17 in PMNs during bacterial infection, we infected mice withE. coliintraperitoneally to establish a septic peritonitis model for studying the PMNs response in peritoneal cavity. We found that PMNs and some of “giant cells” were massively accumulated in the peritoneal cavity of mice with fatal septic peritonitis induced byE. coli. Kinetically, the

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Ishimaru, Naozumi, Kunihiro Otsuka, Takaaki Tsunematsu, Yuhji Taquahashi, and Jun Kanno. "149 Chronic Immunotoxicity of Multi-Walled Carbon Nanotubes on Macrophages via MMP-12." Annals of Work Exposures and Health 67, Supplement_1 (2023): i74. http://dx.doi.org/10.1093/annweh/wxac087.178.

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Abstract Background The toxicological effects of nanomaterials, such as multi-walled carbon nanotubes (MWCNTs), on the immune system are considerably understood. However, the precise relationship between long-term exposure to MWCNTs and chronic inflammation remains unclear. Methods and Finding In this study, exposure to Taquann-treated MWCNTs (T-CNTs) was performed using aerosols generated in an inhalation chamber. At 12 months after T-CNT exposure, alveolar inflammation with macrophage accumulation and hypertrophy of the alveolar walls were observed. The fibrotic lesions were enhanced by T-CN

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Tang, Hung-Jen, Wen-Chien Ko, Chi-Chung Chen, et al. "In Vitro and In Vivo Intracellular Killing Effects of Tigecycline against Clinical Nontyphoid Salmonella Isolates Using Ceftriaxone as a Comparator." Antimicrobial Agents and Chemotherapy 55, no. 6 (2011): 2755–59. http://dx.doi.org/10.1128/aac.01807-10.

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ABSTRACTSalmonellais an important, worldwide food-borne pathogen. Resistance to fluoroquinolones and cephalosporins has been increasingly reported, and new therapeutic agents are desperately needed. In this study, we evaluated thein vitroantimicrobial susceptibility of clinical nontyphoidalSalmonellaisolates to tigecycline. Antibacterial activity of tigecycline, ceftriaxone, and ciprofloxacin were investigated by time-kill studies and the murine peritonitis model. The MIC50/MIC90values of tigecycline, ceftriaxone, and ciprofloxacin against 76Salmonellaisolates were 0.25/0.5, 1/8, and 0.125/0.5

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Morioka, Shin, Kiyomi Nigorikawa, Junko Sasaki, et al. "Myeloid cell-specific inositol polyphosphate-4-phosphatase type I knockout mice impair bacteria clearance in a murine peritonitis model." Innate Immunity 22, no. 6 (2016): 444–51. http://dx.doi.org/10.1177/1753425916652714.

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Phosphatidylinositol 3-kinase (PI3K)/Akt signaling has been implicated in the anti-inflammatory response in a mouse model of endotoxemia and sepsis. The present study focused on the role of inositol polyphosphate-4-phosphatase type I (Inpp4a), which dephosphorylates PtdIns(3,4)P2 to PtdIns(3)P, in bacterial infections. We prepared myeloid cell-specific Inpp4a-conditional knockout mice. Macrophages from these mice showed increased Akt phosphorylation and reduced production of inflammatory cytokines in response to LPS or Escherichia coli in vitro. The Inpp4a knockout mice survived for a shorter

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Ulyanova, Tatiana, Ena R. Banerjee, Gregory V. Priestley, Linda Scott, and Thalia Papayannopoulou. "Migration Defects of Leukocytes from Alpha4 or Beta2 Integrin-Deficient Mice during Aseptic Peritonitis." Blood 104, no. 11 (2004): 2387. http://dx.doi.org/10.1182/blood.v104.11.2387.2387.

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Abstract Leukocyte migration to the inflammatory sites involves a dynamic and coordinated sequence of adhesion/ migration events, in which the α4 and β2 integrins in leukocytes play critical roles. In a model of aseptic peritonitis, normal mice respond with an initial influx of neutrophils followed by later recruitment of mononuclear cells. Previous studies used antibodies to inhibit α4 integrins in this model and provided only early observations (up to 24 hrs). Events at later stages were not addressed. To clarify the role of α4 integrins in this process, we induced aseptic peritonitis in α4-

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Celik, Ilhan, Cordula Stover, Marina Botto, et al. "Role of the Classical Pathway of Complement Activation in Experimentally Induced Polymicrobial Peritonitis." Infection and Immunity 69, no. 12 (2001): 7304–9. http://dx.doi.org/10.1128/iai.69.12.7304-7309.2001.

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ABSTRACT The complement system and the natural antibody repertoire provide a critical first-line defense against infection. The binding of natural antibodies to microbial surfaces opsonizes invading microorganisms and activates complement via the classical pathway. Both defense systems cooperate within the innate immune response. We studied the role of the complement system in the host defense against experimental polymicrobial peritonitis using mice lacking either C1q or factor B and C2. The C1q-deficient mice lacked the classical pathway of complement activation. The factor B- and C2-deficie

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Echtenacher, Bernd, Karin Weigl, Norbert Lehn, and Daniela N. Männel. "Tumor Necrosis Factor-Dependent Adhesions as a Major Protective Mechanism Early in Septic Peritonitis in Mice." Infection and Immunity 69, no. 6 (2001): 3550–55. http://dx.doi.org/10.1128/iai.69.6.3550-3555.2001.

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ABSTRACT The occurrence of peritoneal adhesions in surgical patients is positively correlated with tumor necrosis factor (TNF) levels. In a model of septic peritonitis—cecal ligation and puncture—TNF neutralization prevented formation of peritoneal adhesions and increased mortality, most likely because localization of the septic focus was prevented. To discriminate between the coagulation-independent protective TNF effect and a potential protective procoagulant TNF effect, formation of peritoneal adhesions after CLP was inhibited with heparin, hirudin, or urokinase. Each treatment increased mo

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Bahrami, Maryam, Ali Ghazavi, Ali Ganji, and Ghasem Mosayebi. "Observing the Anti-oxidant and Anti-inflammatory Effect of Nigella Sativa Combined With Silybum Marianum Extracts on the Acute Peritonitis Mouse Model." Journal of Arak University Medical Sciences 24, no. 3 (2021): 372–85. http://dx.doi.org/10.32598/jams.24.3.6154.1.

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Background and Aim: In addition to free radicals such as Nitric Oxide (NO), inflammation is one of the most important pathophysiological causes of peritonitis. Over thousands of years, Nigella Sativa (NS) and Silybum Marianum (SM) are two plants known for their anti-oxidant and anti-inflammatory properties. However, the effect of its compound is unclear. Thus, in this study, we evaluated the anti-inflammatory effect of NS and SM extracts and their combination on inflammatory diseases like thioglycollate peritoneal. Methods & Materials: Alcoholic extracts of SM and NS were obtained by the s

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Mullins, Eric S., Maureen A. Shaw, Zhen Gao та Matthew J. Flick. "Plasmin-Mediated Fibrinolysis Enables Macrophage Migration Via Liberation from Fibrin-αMβ2 Interactions". Blood 132, Supplement 1 (2018): 136. http://dx.doi.org/10.1182/blood-2018-99-117018.

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Abstract Mounting evidence ties both fibrin(ogen) and plasmin(ogen) to inflammatory diseases. Indeed, both fibrin(ogen) and plasmin(ogen) have been linked to critical macrophage functions in multiple disease processes. Migration of macrophages to sites of sterile inflammation is, at least partially, dependent on plasmin(ogen). Mice lacking plasminogen, when challenged with sterile thioglycollate-induced peritonitis, have both diminished overall leukocyte migration and decreased macrophage migration. Additionally, macrophage migration defects have been identified in both mice lacking plasminoge

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Lee, H. Thomas, Mihwa Kim, Jin Deok Joo, George Gallos, Jiang-Fan Chen, and Charles W. Emala. "A3 adenosine receptor activation decreases mortality and renal and hepatic injury in murine septic peritonitis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (2006): R959—R969. http://dx.doi.org/10.1152/ajpregu.00034.2006.

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The role of A3 adenosine receptors (ARs) in sepsis and inflammation is controversial. In this study, we determined the effects of A3AR modulation on mortality and hepatic and renal dysfunction in a murine model of sepsis. To induce sepsis, congenic A3AR knockout mice (A3AR KO) and wild-type control (A3AR WT) mice were subjected to cecal ligation and double puncture (CLP). A3AR KO mice had significantly worse 7-day survival compared with A3AR WT mice. A3AR KO mice also demonstrated significantly higher elevations in plasma creatinine, alanine aminotransferase, aspartate aminotransferase, kerati

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Shi, Ming, XIAOJUN ZHANG, KAI FU, et al. "MARVELD1 promotes survival during septic shock in mice." Journal of Immunology 200, no. 1_Supplement (2018): 109.26. http://dx.doi.org/10.4049/jimmunol.200.supp.109.26.

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Abstract MARVELD1 is integral to the inflammatory response occurring during septic shock, although its precise function has yet to be determined. Here we show that compared with wildtype mice, listeria monocytogenes (LM)-induced septic shock in MARVELD1 knockout mice resulted in a heightened pro-inflammatory response and increased mortality. This observation was associated with impaired bacterial clearance related to marked inhibition of the macrophage phagocytic acitivity in MARVELD1 knockout mice. Consistently, the MARVELD1 knockout mice were more sensitive to a lethal endotoxin or LM challe

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Manuilov, M. B., A. V. Martynov, N. I. Sklyar, V. V. Minukhin, M. S. Biryukov, and A. M. Manuilov. "IOON ONE MED Device Generates Singlet Hydrogen and Active Chlorine to Exhibit Antimicrobial Activity – an Experimental Study." Mikrobiolohichnyi Zhurnal 86, no. 6 (2024): 42–54. https://doi.org/10.15407/microbiolj86.06.042.

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The aim of the study was to investigate the in vitro antimicrobial activity against museum and circulating strains of microorganisms and fungi of an aqueous solution generated by the IOON ONE MED device containing atomic hydrogen and atomic (active) chlorine at a concentration of 1 mg/L as active substances and in vivo on a standardized model of purulent peritonitis in two variants – prophylactic (neutralization of bacteria) and therapeutic (effect on advanced infection). Methods. Microbiological methods were used to study the antimicrobial activity of new substances in vitro on museum and cir

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Knudsen, Jenny Dahl, Kurt Fuursted, Susan Raber, Frank Espersen, and Niels Frimodt-Møller. "Pharmacodynamics of Glycopeptides in the Mouse Peritonitis Model of Streptococcus pneumoniae orStaphylococcus aureus Infection." Antimicrobial Agents and Chemotherapy 44, no. 5 (2000): 1247–54. http://dx.doi.org/10.1128/aac.44.5.1247-1254.2000.

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ABSTRACT The emergence of resistance to various antibiotics in pneumococci leaves the glycopeptides as the only antibiotics against which pneumococci have no resistance mechanism. This situation has led to a renewed interest in the use of glycopeptides. It has not yet been possible to conclude which one or more of the pharmacokinetic or pharmacodynamic (PK/PD) parameters are the most important and best predictors for the effects of treatment with glycopeptides in animal models or in humans. We used the mouse peritonitis model with immunocompetent mice and with Staphylococcus aureus and Strepto

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Aragão, Gislei Frota, Dayanne Terra Tenório Nonato, Edson Lopes da Ponta, et al. "Protective effects of ethanolic extract from the red algae Amansia multifida on experimental inflammation, nociception and seizure experimental models." Acta Scientiarum. Biological Sciences 38, no. 4 (2016): 465. http://dx.doi.org/10.4025/actascibiolsci.v38i4.32361.

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This study aimed to investigate the EEAm effect in mice models of nociception, inflammation and in behavioral tests evaluating the central nervous system. EEAm had inhibitory effects in the following tests: acetic acid-induced writhing (78%); formalin (62% - inflammatory phase); open field (46%). EEAm increased the nociceptive latency (56%) in tail flick test and increased the death-latency by 36% in the pentylenetetrazole-induced seizure model. Moreover, EEAm inhibited paw edema (82%) and peritonitis (45%) induced by carrageenan. In conclusion, EEAm presents antinociceptive, anti-inflammatory

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