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Journal articles on the topic 'Lavagem de rolhas'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Elahi, S., R. Brownlie, J. Korzeniowski, et al. "Infection of Newborn Piglets with Bordetella pertussis: a New Model for Pertussis." Infection and Immunity 73, no. 6 (2005): 3636–45. http://dx.doi.org/10.1128/iai.73.6.3636-3645.2005.

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ABSTRACT Bordetella pertussis is the causative agent of pertussis or whooping cough. This bacterium is a human pathogen that under experimental conditions also infects selected rodents and primates. Here, we show for the first time that newborn piglets can be infected with B. pertussis when it is delivered intrapulmonarily. Infected piglets displayed fever and respiratory symptoms, such as nasal discharge, nonparoxysmal coughing, and breathing difficulties. Eventually, all infected animals developed severe bronchopneumonia, which in some cases was combined with a fibrinous pleuritits. Immunohi

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Komori, Masashi, Hiromasa Inoue, Koichiro Matsumoto, et al. "PAF mediates cigarette smoke-induced goblet cell metaplasia in guinea pig airways." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 3 (2001): L436—L441. http://dx.doi.org/10.1152/ajplung.2001.280.3.l436.

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Goblet cell metaplasia is an important morphological feature in the airways of patients with chronic airway diseases; however, the precise mechanisms that cause this feature are unknown. We investigated the role of endogenous platelet-activating factor (PAF) in airway goblet cell metaplasia induced by cigarette smoke in vivo. Guinea pigs were exposed repeatedly to cigarette smoke for 14 consecutive days. The number of goblet cells in each trachea was determined with Alcian blue-periodic acid-Schiff staining. Differential cell counts and PAF levels in bronchoalveolar lavage fluid were also eval

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Gahlot, Luxmi, Francis H. Y. Green, Anita Rigaux, Jennifer M. Schneider, and Shabih U. Hasan. "Role of vagal innervation on pulmonary surfactant system during fetal development." Journal of Applied Physiology 106, no. 5 (2009): 1641–49. http://dx.doi.org/10.1152/japplphysiol.90868.2008.

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Vagally mediated afferent feedback and compliant lungs (surfactant system) play vital roles in the establishment of adequate alveolar ventilation and pulmonary gas exchange at birth. Although the significance of vagal innervation in the establishment of normal breathing patterns is well recognized, the precise role of lung innervation in the maturation of the surfactant system remains unclear. The specific aim of the present study was to investigate whether vagal denervation compromises the surfactant system during fetal development. Experiments were performed on 12 time-dated fetal sheep: 8 u

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4

Wilson, Michael R., Sharmila Choudhury, and Masao Takata. "Pulmonary inflammation induced by high-stretch ventilation is mediated by tumor necrosis factor signaling in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 4 (2005): L599—L607. http://dx.doi.org/10.1152/ajplung.00304.2004.

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Although high-stretch mechanical ventilation has been demonstrated to induce lung inflammation, the roles of soluble mediators, in particular TNF, remain controversial. We have previously shown in mice that high-stretch ventilation, in the absence of preceding lung injury, induces expression of bioactive TNF in lung lavage fluid early in the course of injury, but the biological significance of this, if any, has yet to be determined. We therefore investigated the pulmonary inflammatory response to a transient period of high-stretch ventilation in anesthetized mice lacking TNF receptors and mice

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5

Paananen, Reija, Raija Sormunen, Virpi Glumoff, Martin van Eijk, and Mikko Hallman. "Surfactant proteins A and D in Eustachian tube epithelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 281, no. 3 (2001): L660—L667. http://dx.doi.org/10.1152/ajplung.2001.281.3.l660.

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Surfactant protein (SP) A and SP-D are collectins that have roles in host defense. The Eustachian tube (ET) maintains the patency between the upper airways and the middle ear. Dysfunction of local mucosal immunity in ET may predispose infants to recurrent otitis media. We recently described preliminary evidence of the expression of SP-A and SP-D in the ET. Our present aim was to establish the sites of SP-A and SP-D expression within the epithelium of the ET in vivo. With in situ hybridization, electron microscopy, and immunoelectron microscopy, the cells responsible for SP-A and SP-D expressio

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6

Shi, Ying, Jian Dai, Hua Liu та ін. "Naringenin inhibits allergen-induced airway inflammation and airway responsiveness and inhibits NF-κB activity in a murine model of asthma". Canadian Journal of Physiology and Pharmacology 87, № 9 (2009): 729–35. http://dx.doi.org/10.1139/y09-065.

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Naringenin, a flavonoid, has antiinflammatory and immunomodulatory properties. We investigated whether naringenin could attenuate allergen-induced airway inflammation and its possible mechanism in a murine model of asthma. Mice were sensitized and challenged with ovalbumin. Some mice were administered with naringenin before ovalbumin challenge. We evaluated the development of airway inflammation and airway reactivity. Interleukin (IL)4, IL13, chemokine (C–C motif) ligand (CCL)5, and CCL11 in bronchoalveolar lavage fluid and serum total IgE were detected by ELISA. IκBα degradation and inducible

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7

Bartlett, Jennifer A., Matthew E. Albertolle, Christine Wohlford-Lenane, et al. "Protein composition of bronchoalveolar lavage fluid and airway surface liquid from newborn pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 3 (2013): L256—L266. http://dx.doi.org/10.1152/ajplung.00056.2013.

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The airway mucosa and the alveolar surface form dynamic interfaces between the lung and the external environment. The epithelial cells lining these barriers elaborate a thin liquid layer containing secreted peptides and proteins that contribute to host defense and other functions. The goal of this study was to develop and apply methods to define the proteome of porcine lung lining liquid, in part, by leveraging the wealth of information in the Sus scrofa database of Ensembl gene, transcript, and protein model predictions. We developed an optimized workflow for detection of secreted proteins in

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8

Lalani, Salim, John E. Remmers, Yolanda MacKinnon, Gordon T. Ford, and Shabih U. Hasan. "Hypoxemia and low Crs in vagally denervated lambs result from reduced lung volume and not pulmonary edema." Journal of Applied Physiology 93, no. 2 (2002): 601–10. http://dx.doi.org/10.1152/japplphysiol.00949.2001.

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Vagal denervation performed in the intrathoracic region in newborn lambs leads to hypoxemia and decreased respiratory system compliance (Crs), which could result from atelectasis and/or pulmonary edema. The objective of the present study was to quantify the relative roles of alveolar derecruitment and pulmonary edema as underlying cause(s) of respiratory failure. Vagal denervation was performed in the intrathoracic region and below the recurrent laryngeal nerves in six newborn lambs within 24 h of birth, whereas six were sham operated. Pre- and postinflation Crs was measured to investigate the

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9

Godshall, Christopher J., Alex B. Lentsch, James C. Peyton, Melanie J. Scott, and William G. Cheadle. "STAT4 Is Required for Antibacterial Defense but Enhances Mortality during Polymicrobial Sepsis." Clinical Diagnostic Laboratory Immunology 8, no. 6 (2001): 1044–48. http://dx.doi.org/10.1128/cdli.8.6.1044-1048.2001.

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ABSTRACT The signal transducer and activator of transcription factor 4 (STAT4) pathway mediates the intracellular effects of interleukin-12 (IL-12), leading to the production of gamma interferon, induction of a T helper type 1 response, and increased natural killer cell cytotoxicity. The purpose of this study was to determine the role of the STAT4 pathway during polymicrobial peritonitis in the cecal ligation and puncture (CLP) model. CLP was performed on STAT4-deficient (STAT4−/−) and wild-type control (BALB/c) mice. At 4 h after CLP, STAT4−/− mice had significantly higher bacterial counts in

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10

Ebina, Masahito, Hiroyuki Taniguchi, Taku Miyasho, et al. "Gradual Increase of High Mobility Group Protein B1 in the Lungs after the Onset of Acute Exacerbation of Idiopathic Pulmonary Fibrosis." Pulmonary Medicine 2011 (2011): 1–9. http://dx.doi.org/10.1155/2011/916486.

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The pathogenesis of acute exacerbation of idiopathic pulmonary fibrosis (IPF) remains to be elucidated. To evaluate the roles of inflammatory mediators in acute exacerbation, the concentrations of high mobility group protein B1 (HMGB1), a chief mediator of acute lung injury, and 18 inflammatory cytokines were measured in the bronchoalveolar lavage fluid, serially sampled from seven IPF patients after the onset of acute exacerbation. HMGB1 gradually increased in the alveolar fluid after the onset of acute exacerbation, in positive correlation with monocytes chemotactic protein-1 (MCP-1), a pote

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11

Kleeberger, S. R., J. Kolbe, N. F. Adkinson, S. P. Peters, and E. W. Spannhake. "Central role of cyclooxygenase in the response of canine peripheral airways to antigen." Journal of Applied Physiology 61, no. 4 (1986): 1309–15. http://dx.doi.org/10.1152/jappl.1986.61.4.1309.

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We studied the effects of antigen aerosol challenge on the airways of the canine peripheral lung and examined the roles of cyclooxygenase products, histamine, and cholinergic activity in the responses. One-minute deliveries of 1:10,000 or 1:100,000 concentrations of Ascaris suum antigen aerosol through a wedged bronchoscope resulted in mean maximal increases in collateral system resistance (Rcs) of 415 and 177%, respectively, after 4–8 min. Repeated antigen challenge (1:100,000) resulted in significantly decreased responsiveness to antigen after the initial exposure (P less than 0.005). Bronch

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12

Aoki-Nagase, Tomoko, Takahide Nagase, Yoshio Oh-hashi, et al. "Attenuation of antigen-induced airway hyperresponsiveness in CGRP-deficient mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 5 (2002): L963—L970. http://dx.doi.org/10.1152/ajplung.00130.2002.

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Bronchial hyperresponsiveness and eosinophilia are major characteristics of asthma. Calcitonin gene-related peptide (CGRP) is a neuropeptide that has various biological actions. In the present study, we questioned whether CGRP might have pathophysiological roles in airway hyperresponsiveness and eosinophilia in asthma. To determine the exact roles of endogenous CGRP in vivo, we chose to study antigen-induced airway responses using CGRP gene-disrupted mice. After ovalbumin sensitization and antigen challenge, we assessed airway responsiveness and measured proinflammatory mediators. In the sensi

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13

Nagano, Tatsuya, Masahiro Katsurada, Ryota Dokuni, et al. "Crucial Role of Extracellular Vesicles in Bronchial Asthma." International Journal of Molecular Sciences 20, no. 10 (2019): 2589. http://dx.doi.org/10.3390/ijms20102589.

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Extracellular vesicles (EVs) are circulating vesicles secreted by various cell types. EVs are classified into three groups according to size, structural components, and generation process of vesicles: exosomes, microvesicles, and apoptotic bodies. Recently, EVs have been considered to be crucial for cell-to-cell communications and homeostasis because they contain intracellular proteins and nucleic acids. Epithelial cells from mice suffering from bronchial asthma (BA) secrete more EVs and suppress inflammation-induced EV production. Moreover, microarray analyses of bronchoalveolar lavage fluid

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14

Bergallo, Massimiliano, Cristina Costa, Maria Elena Terlizzi, et al. "Development of a LUX real-time PCR for the detection and quantification of human herpesvirus 7." Canadian Journal of Microbiology 55, no. 3 (2009): 319–25. http://dx.doi.org/10.1139/w08-134.

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Human herpesvirus 7 is a highly seroprevalent β-herpesvirus that, following primary infection, remains latent in CD4+ T cells and determines a persistent rather than a latent infection in various tissues and organs, including the lung and skin. This paper describes the development of an in-house light upon extension real-time PCR assay for quantification of human herpesvirus 7 DNA in clinical samples. The efficiency, sensitivity, specificity, inter- and intra-assay variability, and dynamic range have been determined. Subsequently, the assay has been validated by evaluating the human herpesviru

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15

Yoshikawa, Sawako, Takashige Miyahara, Susan D. Reynolds, et al. "Clara cell secretory protein and phospholipase A2 activity modulate acute ventilator-induced lung injury in mice." Journal of Applied Physiology 98, no. 4 (2005): 1264–71. http://dx.doi.org/10.1152/japplphysiol.01150.2004.

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Lung vascular permeability is acutely increased by high-pressure and high-volume ventilation. To determine the roles of mechanically activated cytosolic PLA2 (cPLA2) and Clara cell secretory protein (CCSP), a modulator of cPLA2 activity, we compared lung injury with and without a PLA2 inhibitor in wild-type mice and CCSP-null mice (CCSP−/−) ventilated with high and low peak inflation pressures (PIP) for 2- or 4-h periods. After ventilation with high PIP, we observed significant increases in the bronchoalveolar lavage albumin concentrations, lung wet-to-dry weight ratios, and lung myeloperoxida

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16

Tong, Hua Hua, Yong Xing Li, Gregory L. Stahl, and Joshua M. Thurman. "Enhanced Susceptibility to Acute Pneumococcal Otitis Media in Mice Deficient in Complement C1qa, Factor B, and Factor B/C2." Infection and Immunity 78, no. 3 (2010): 976–83. http://dx.doi.org/10.1128/iai.01012-09.

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ABSTRACT To define the roles of specific complement activation pathways in host defense against Streptococcus pneumoniae in acute otitis media (AOM), we investigated the susceptibility to AOM in mice deficient in complement factor B and C2 (Bf/C2 −/ −), C1qa (C1qa −/ −), and factor B (Bf − / −). Bacterial titers of both S. pneumoniae serotype 6A and 14 in the middle ear lavage fluid samples from Bf/C2 −/ −, Bf − / −, and C1qa −/ − mice were significantly higher than in samples from wild-type mice 24 h after transtympanical infection (P < 0.05) and remained persistently higher in samples fro

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17

Sozo, Foula, Melissa Vela, Victoria Stokes, et al. "Effects of prenatal ethanol exposure on the lungs of postnatal lambs." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 1 (2011): L139—L147. http://dx.doi.org/10.1152/ajplung.00195.2010.

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Prenatal ethanol exposure increases collagen deposition and alters surfactant protein (SP) expression and immune status in lungs of near-term fetal sheep. Our objectives were to determine 1) whether these prenatal effects of repeated gestational ethanol exposure persist after birth and 2) whether surfactant phospholipid composition is altered following prenatal ethanol exposure. Pregnant ewes were chronically catheterized at 90 days of gestational age (DGA) and given a 1-h daily infusion of ethanol (0.75 g/kg, n = 9) or saline ( n = 7) from 95 to 135 DGA; ethanol administration ceased after 13

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18

Nikkhoo, Bahram, Naseh Sigari, Bayazid Ghaderi, et al. "Diagnostic Utility of Adenosine Deaminase in Serum and Bronchoalveolar Lavage Fluid for Screening Lung Cancer in Western Iran." Journal of Medical Biochemistry 32, no. 2 (2013): 109–15. http://dx.doi.org/10.2478/jomb-2013-0011.

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Summary Background: This study aimed to determine adenosine deaminase (ADA) activity as a possible screening tool in lung cancer patients. Methods: Blood samples were collected from 30 subjects with positive pathological tests and 62 patients with negative pathological tests as a control group. The enzymatic activity of total ADA and its isoenzymes was determined. Results: tADA and ADA2 isoenzyme activity was significantly higher in cancerous patients compared to benign controls in serum and BAL fluid. Using a cut-off level of respectively 35.22 U/L and 31.80 U/L for BAL total ADA and ADA2, se

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19

Shirasaki, Hideaki, Etsuko Kanaizumi, and Tetsuo Himi. "Immunohistochemical Localization of the Bradykinin B1 and B2 Receptors in Human Nasal Mucosa." Mediators of Inflammation 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/102406.

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Bradykinin (BK) has been tobe thought a potent mediator involved in allergic rhinitis because BK was recovered from the nasal lavage fluid of allergic rhinitis patients after allergen provocation and BK receptor antagonists relief nasal allergic symptoms. Two mammalian BK receptor subtypes, B1 and B2, have been defined based on their pharmacological properties. We investigated the localization of these receptors by immunohistochemistry. Human turbinates were obtained after turbinectomy from 12 patients with nasal obstruction refractory to medical therapy. The immunohistochemical study revealed

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Hopkins, H. A., M. M. Monick, and G. W. Hunninghake. "Lipopolysaccharide upregulates surface expression of CD14 on human alveolar macrophages." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 6 (1995): L849—L854. http://dx.doi.org/10.1152/ajplung.1995.269.6.l849.

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This study was undertaken to examine the surface expression and regulation of CD14 on human alveolar macrophages (HAM). HAM obtained by bronchoalveolar lavage were cultured with or without LPS and with or without fetal bovine serum (FBS) on plastic or Teflon surfaces. CD14 expression was assessed by immunofluorescence. The roles of protein tyrosine kinase, protein kinase A, and protein kinase C were also evaluated utilizing inhibitors of these enzymes. HAM expressed very low levels of surface CD14 at baseline. CD14 was upregulated on HAM with time in culture in the presence of FBS and/or LPS;

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21

Ofulue, A. Felix, and Mary Ko. "Effects of depletion of neutrophils or macrophages on development of cigarette smoke-induced emphysema." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 1 (1999): L97—L105. http://dx.doi.org/10.1152/ajplung.1999.277.1.l97.

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The aim of this study was to ascertain the putative roles of neutrophils or macrophages in the pathogenesis of cigarette smoking-induced emphysema on the basis of effects of anti-neutrophil (anti-PMN) antibody or anti-monocyte/macrophage (anti-MoMac) antibody on the development of emphysema in cigarette smoke-exposed rats. Rats were treated with rabbit anti-PMN or anti-MoMac antibody and exposed 7 days/wk for 2 mo to cigarette smoke inhalation; rats treated with nonimmunized rabbit IgG (control antibody) and exposed to cigarette smoke or normal room air served as controls. Antibody treatments

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22

Scott, C. L., D. A. Hughes, D. Cary, N. A. Nicola, C. G. Begley та L. Robb. "Functional Analysis of Mature Hematopoietic Cells From Mice Lacking the βc Chain of the Granulocyte-Macrophage Colony-Stimulating Factor Receptor". Blood 92, № 11 (1998): 4119–27. http://dx.doi.org/10.1182/blood.v92.11.4119.

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Abstract Mice with a null mutation of the βc chain of the granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5 receptors (βc-null mice) develop an alveolar proteinosis-like lung disease. The pathogenesis of this disease is uncertain and, although a defect in alveolar macrophage function has been postulated, no previous analysis of mature hematopoietic cells in mice with alveolar proteinosis has been reported. Therefore, we undertook a functional analysis of the mature hematopoietic cell compartment in βc-null mice. In addition, we reexamined the roles of th

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Scott, C. L., D. A. Hughes, D. Cary, N. A. Nicola, C. G. Begley та L. Robb. "Functional Analysis of Mature Hematopoietic Cells From Mice Lacking the βc Chain of the Granulocyte-Macrophage Colony-Stimulating Factor Receptor". Blood 92, № 11 (1998): 4119–27. http://dx.doi.org/10.1182/blood.v92.11.4119.423k40_4119_4127.

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Mice with a null mutation of the βc chain of the granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-3 (IL-3), and IL-5 receptors (βc-null mice) develop an alveolar proteinosis-like lung disease. The pathogenesis of this disease is uncertain and, although a defect in alveolar macrophage function has been postulated, no previous analysis of mature hematopoietic cells in mice with alveolar proteinosis has been reported. Therefore, we undertook a functional analysis of the mature hematopoietic cell compartment in βc-null mice. In addition, we reexamined the roles of the GM-CSF

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Banerjee, Antara, Frederik Stevenaert, Kalyan Pande, et al. "Modulation of Paired Immunoglobulin-Like Type 2 Receptor Signaling Alters the Host Response to Staphylococcus aureus-Induced Pneumonia." Infection and Immunity 78, no. 3 (2010): 1353–63. http://dx.doi.org/10.1128/iai.00969-09.

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ABSTRACT Paired immunoglobulin-like type 2 receptors (PILRs) inhibitory PILRα and activating PILRβ are predominantly expressed on myeloid cells. Their functions in host defense and inflammation are largely unknown, and in this study, we evaluated their roles in an acute Staphylococcus aureus pneumonia model. Compared to their respective controls, Pilrb −/− mice or mice in which PILRα was activated with an agonistic antibody showed improved clearance of pulmonary staphylococci and improved survival. These mice had reduced serum or bronchoalveolar lavage fluid levels of interleukin-1β (IL-1β), t

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Vaneker, Michiel, Leo A. Joosten, Leo M. A. Heunks, et al. "Low-tidal-volume Mechanical Ventilation Induces a Toll-like Receptor 4–dependent Inflammatory Response in Healthy Mice." Anesthesiology 109, no. 3 (2008): 465–72. http://dx.doi.org/10.1097/aln.0b013e318182aef1.

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Background Mechanical ventilation (MV) can induce ventilator-induced lung injury. A role for proinflammatory pathways has been proposed. The current studies analyzed the roles of Toll-like receptor (TLR) 4 and TLR2 involvement in the inflammatory response after MV in the healthy lung. Methods Wild-type (WT) C57BL6, TLR4 knockout (KO), and TLR2 KO mice were mechanically ventilated for 4 h. Bronchoalveolar lavage fluid was analyzed for presence of endogenous ligands. Lung homogenates were used to investigate changes in TLR4 and TLR2 expression. Cytokines were measured in lung homogenate and plas

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Liu, Yu, Rong Lin, Xiaolian Shi, et al. "The Roles of Buyang Huanwu Decoction in Anti-Inflammation, Antioxidation and Regulation of Lipid Metabolism in Rats with Myocardial Ischemia." Evidence-Based Complementary and Alternative Medicine 2011 (2011): 1–8. http://dx.doi.org/10.1093/ecam/neq028.

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Buyang Huanwu Decoction (BYHWD) is a well-known Chinese medicine formula. Recent studies have reported that BYHWD can be used to treat ischemic heart disease. This study investigated the potential mechanism underlying the roles of BYHWD in alleviating the myocardial ischemia induced by isoproterenol (ISO) in rats. Different doses of BYHWD (25.68, 12.84 and 6.42 g kg−1) were lavaged to rats, respectively. Then the expression of the cluster of differentiation 40 (CD40) in the mononuclear cells was measured using flow cytometry, and the expressions of CD40 and its ligand (CD40L) in myocardial tis

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Zhang, Guqin, Hanxiang Nie, Jiong Yang, et al. "Sulfatide-activated type II NKT cells prevent allergic airway inflammation by inhibiting type I NKT cell function in a mouse model of asthma." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 6 (2011): L975—L984. http://dx.doi.org/10.1152/ajplung.00114.2011.

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Asthma is a common chronic inflammatory disease involving many different cell types. Recently, type I natural killer T (NKT) cells have been demonstrated to play a crucial role in the development of asthma. However, the roles of type II NKT cells in asthma have not been investigated before. Interestingly, type I and type II NKT cells have been shown to have opposing roles in antitumor immunity, antiparasite immunity, and autoimmunity. We hypothesized that sulfatide-activated type II NKT cells could prevent allergic airway inflammation by inhibiting type I NKT cell function in asthma. Strikingl

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Bless, Nicolas M., Roscoe L. Warner, Vaishalee A. Padgaonkar, et al. "Roles for C-X-C chemokines and C5a in lung injury after hindlimb ischemia-reperfusion." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 1 (1999): L57—L63. http://dx.doi.org/10.1152/ajplung.1999.276.1.l57.

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We evaluated the roles of the C-X-C chemokines cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) as well as the complement activation product C5a in development of lung injury after hindlimb ischemia-reperfusion in rats. During reperfusion, CD11b and CD18, but not CD11a, were upregulated on neutrophils [bronchoalveolar lavage (BAL) and blood] and lung macrophages. BAL levels of CINC and MIP-2 were increased during the ischemic and reperfusion periods. Treatment with either anti-CINC or anti-MIP-2 IgG significantly reduced lung vascular permeabilit

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Oshima, Ken-Zaburo, Kazuhito Asano, Ken-Ichi Kanai, Miyuki Suzuki, and Harumi Suzaki. "Influence of Epinastine Hydrochloride, an -Receptor Antagonist, on the Function of Mite Allergen-Pulsed Murine Bone Marrow-Derived Dendritic Cells In Vitro and In Vivo." Mediators of Inflammation 2009 (2009): 1–8. http://dx.doi.org/10.1155/2009/738038.

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There is established concept that dendritic cells (DCs) play essential roles in the development of allergic immune responses. However, the influence of receptor antagonists on DC functions is not well defined. The aim of the present study was to examine the effect of epinastine hydrochloride (EP), the most notable histamine receptor antagonists in Japan, onDermatophagoides farinae (Der f)-pulsed mouse bone marrow-derived DCs in vitro and in vivo. EP at more than 25 ng/mL could significantly inhibit the production of IL-6, TNF- and IL-10 fromDer f-pulsed DCs, which was increased byDer fchalleng

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Xu, Younian, Chen Meng, Guilin Liu, et al. "Classically Activated Macrophages Protect against Lipopolysaccharide-induced Acute Lung Injury by Expressing Amphiregulin in Mice." Anesthesiology 124, no. 5 (2016): 1086–99. http://dx.doi.org/10.1097/aln.0000000000001026.

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Abstract Background Alveolar macrophages (AMs) activated into M1 phenotype are involved in the development of lipopolysaccharide-induced acute lung injury (ALI). However, whether AMs express amphiregulin and what roles amphiregulin plays in lipopolysaccharide-induced ALI remain poorly understood. Methods Acute lung injury was induced by intratracheal instillation of lipopolysaccharide in male C57BL/6 mice. Lung injury scores, level of protein, and level of neutrophils in bronchial alveolar lavage fluid of lipopolysaccharide-induced ALI mice were compared with those in mice challenged with reco

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Tanino, Yoshinori, Xintao Wang, Takefumi Nikaido та ін. "Syndecan-4 Inhibits the Development of Pulmonary Fibrosis by Attenuating TGF-β Signaling". International Journal of Molecular Sciences 20, № 20 (2019): 4989. http://dx.doi.org/10.3390/ijms20204989.

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Syndecan-4 is a transmembrane heparan sulfate proteoglycan expressed in a variety of cells, and its heparan sulfate glycosaminoglycan side chains bind to several proteins exhibiting various biological roles. The authors have previously demonstrated syndecan-4′s critical roles in pulmonary inflammation. In the current study, however, its role in pulmonary fibrosis was evaluated. Wild-type and syndecan-4-deficient mice were injected with bleomycin, and several parameters of inflammation and fibrosis were analyzed. The mRNA expression of collagen and α-smooth muscle action (α-SMA) in lung tissues

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Skerrett, Shawn J., Thomas R. Martin, Emil Y. Chi, Jacques J. Peschon, Kendall M. Mohler, and Christopher B. Wilson. "Role of the type 1 TNF receptor in lung inflammation after inhalation of endotoxin orPseudomonas aeruginosa." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (1999): L715—L727. http://dx.doi.org/10.1152/ajplung.1999.276.5.l715.

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To determine the roles of the type 1 tumor necrosis factor (TNF) receptor (TNFR1) in lung inflammation and antibacterial defense, we exposed transgenic mice lacking TNFR1 [TNFR1(−/−)] and wild-type control mice to aerosolized lipopolysaccharide or Pseudomonas aeruginosa. After LPS, bronchoalveolar lavage fluid (BALF) from TNFR1(−/−) mice contained fewer neutrophils and less macrophage inflammatory protein-2 than BALF from control mice. TNF-α, interleukin-1β, and total protein levels in BALF as well as tissue intercellular adhesion molecule-1 expression did not differ between the two groups. In

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Jiao, Hao, Jieqiong Song, Xia Sun, Dong Sun, and Ming Zhong. "Sodium Arsenite Inhibits Lung Fibroblast Differentiation and Pulmonary Fibrosis." Pharmacology 104, no. 5-6 (2019): 368–76. http://dx.doi.org/10.1159/000502536.

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Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease with a high mortality and poor prognosis. Transforming growth factor (TGF)-β plays crucial roles in the pathogenesis of IPF. To investigate the role of sodium arsenite (SA) on fibroblast differentiation and pulmonary fibrosis, we checked the effects of SA on TGF-β-induced normal human lung fibroblasts (NHLFs) differentiation, and the anti-fibrotic effect of SA on bleomycin (BLM)-induced pulmonary fibrosis in mouse. SA treatment significantly inhibits α-smooth muscle actin and fibronectin (FN) expression in TGF-β treated

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Liu, Hui-Fang, Hui-Jie Zhang, Qi-Xian Hu, et al. "Altered Polarization, Morphology, and Impaired Innate Immunity Germane to Resident Peritoneal Macrophages in Mice with Long-Term Type 2 Diabetes." Journal of Biomedicine and Biotechnology 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/867023.

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Type 2 diabetes (T2D) is associated with perturbed innate immunity. Macrophages, bridging innate immunity and metabolic disturbances, play important roles in controlling immune homeostasis. However, the effect of long-term diabetic milieu (DM) on the functions and phenotypes of macrophages is still not clear. In this study, we used resident peritoneal macrophages (RPMs) from 5-month-old db/db mice to investigate the changes of macrophages. It was found that RPMs in db/db mice significantly reduced phagocytosis and adhesion capacity. After standardization with body weight, the number of F4/80+

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Caparrós-Martín, Jose A., Stephanie Flynn, F. Jerry Reen, et al. "The Detection of Bile Acids in the Lungs of Paediatric Cystic Fibrosis Patients Is Associated with Altered Inflammatory Patterns." Diagnostics 10, no. 5 (2020): 282. http://dx.doi.org/10.3390/diagnostics10050282.

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Background: Cystic fibrosis (CF) is a hereditary disorder in which persistent unresolved inflammation and recurrent airway infections play major roles in the initiation and progression of the disease. Little is known about triggering factors modulating the transition to chronic microbial infection and inflammation particularly in young children. Cystic fibrosis respiratory disease starts early in life, with the detection of inflammatory markers and infection evident even before respiratory symptoms arise. Thus, identifying factors that dysregulate immune responsiveness at the earliest stages o

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Kanazawa, H., H. Kamoi, T. Kawaguchi, et al. "PAMP is a novel inhibitor of the tachykinin release in the airway of guinea pigs." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 6 (1997): L1066—L1069. http://dx.doi.org/10.1152/ajplung.1997.272.6.l1066.

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Proadrenomedullin NH2-terminal 20 peptide (PAMP), a newly identified hypotensive peptide, may play physiological roles in airway and cardiovascular controls. This study was designed to determine the mechanism responsible for the bronchoprotective effects of PAMP on capsaicin-induced bron-choconstriction in anesthetized guinea pigs. PAMP (10(-8)-10(-6) M) significantly inhibited capsaicin-induced bronchoconstriction in a dose-dependent manner. The bronchoprotective effect of PAMP (10(-6) M) was as large as that of isoproterenol (10(-7) M) and lasted > 10 min. The concentration of immunoreact

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Watkins, Richard H., Carl T. D’Angio, Rita M. Ryan, Alka Patel, and William M. Maniscalco. "Differential expression of VEGF mRNA splice variants in newborn and adult hyperoxic lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (1999): L858—L867. http://dx.doi.org/10.1152/ajplung.1999.276.5.l858.

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Lung development and repair of hyperoxic injury require closely regulated growth and regeneration of alveolar capillaries. Vascular endothelial growth factor (VEGF), a mitogen for endothelial cells, is expressed by alveolar epithelial cells. Alternative splicing of VEGF mRNA results in isoforms of varying mitogenicity and solubility. We examined changes in the proportions of the VEGF splice variant mRNAs in rabbit lung development and in control, oxygen-injured, and recovering newborn and adult rabbit lungs. The proportion of the 189-amino acid VEGF mRNA, which codes for an isoform that binds

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Li, Xuanfei, Zheng Liu, He Jin та ін. "Agmatine Protects against Zymosan-Induced Acute Lung Injury in Mice by Inhibiting NF-κB-Mediated Inflammatory Response". BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/583736.

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Acute lung injury (ALI) is characterized by overwhelming lung inflammation and anti-inflammation treatment is proposed to be a therapeutic strategy for ALI. Agmatine, a cationic polyamine formed by decarboxylation of L-arginine, is an endogenous neuromodulator that plays protective roles in diverse central nervous system (CNS) disorders. Consistent with its neuromodulatory and neuroprotective properties, agmatine has been reported to have beneficial effects on depression, anxiety, hypoxic ischemia, Parkinson’s disease, and gastric disorder. In this study, we tested the effect of agmatine on th

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Zhu, Chen, Qing-Yu Weng, Ling-Ren Zhou, et al. "Homeostatic and early-recruited CD101− eosinophils suppress endotoxin-induced acute lung injury." European Respiratory Journal 56, no. 5 (2020): 1902354. http://dx.doi.org/10.1183/13993003.02354-2019.

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IntroductionAcute lung injury (ALI) is a fatal but undertreated condition with severe neutrophilic inflammation, although little is known about the functions of eosinophils in the pathogenesis of ALI. Our objectives were to investigate the roles and molecular mechanisms of eosinophils in ALI.MethodsPulmonary eosinophils were identified by flow cytometry. Mice with abundant or deficient eosinophils were used. Cellularity of eosinophils and neutrophils in bronchoalveolar lavage fluid, inflammatory assessment, and survival rate were determined. Human samples were also used for validating experime

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Kida, Takashi, Takahiro Seno, Hidetake Nagahara, et al. "Roles of high-mobility group box 1 and thrombin in murine pulmonary fibrosis and the therapeutic potential of thrombomodulin." American Journal of Physiology-Lung Cellular and Molecular Physiology 314, no. 3 (2018): L473—L483. http://dx.doi.org/10.1152/ajplung.00287.2017.

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Cross talk between inflammation and coagulation plays important roles in acute or subacute progressive pulmonary fibrosis characterized by diffuse alveolar damage. Thrombomodulin is a physiological inhibitor of high-mobility group box 1 (HMGB1), and thrombin and may be effective for this condition. This study investigated the roles of HMGB1 and thrombin in the pathophysiology of bleomycin-induced pulmonary fibrosis and the efficacy of recombinant human soluble thrombomodulin (rhTM). Pulmonary fibrosis was induced in wild-type C57BL/6 mice by intratracheal instillation of bleomycin. We first as

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Gauthier, Jean-François, Andrée Fortin, Yves Bergeron, Marie-Christine Dumas, Marie-Eve Champagne, and Michel G. Bergeron. "Differential Contribution of Bacterial N-Formyl-Methionyl-Leucyl- Phenylalanine and Host-Derived CXC Chemokines to Neutrophil Infiltration into Pulmonary Alveoli during Murine Pneumococcal Pneumonia." Infection and Immunity 75, no. 11 (2007): 5361–67. http://dx.doi.org/10.1128/iai.02008-06.

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ABSTRACT Despite the development of new potent antibiotics, Streptococcus pneumoniae remains the leading cause of death from bacterial pneumonia. Polymorphonuclear neutrophil (PMN) recruitment into the lungs is a primordial step towards host survival. Bacterium-derived N-formyl peptides (N-formyl-methionyl-leucyl-phenylalanine [fMLP]) and host-derived chemokines (KC and macrophage inflammatory protein 2 [MIP-2]) are likely candidates among chemoattractants to coordinate PMN infiltration into alveolar spaces. To investigate the contribution of each in the context of pneumococcal pneumonia, CD1,

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Fussbroich, D., R. A. Colas, O. Eickmeier, et al. "A combination of LCPUFA ameliorates airway inflammation in asthmatic mice by promoting pro-resolving effects and reducing adverse effects of EPA." Mucosal Immunology 13, no. 3 (2020): 481–92. http://dx.doi.org/10.1038/s41385-019-0245-2.

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AbstractLipid mediators derived from omega (n)-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA) play key roles in bronchoconstriction, airway inflammation, and resolution processes in asthma. This study compared the effects of dietary supplementation with either a combination of LCPUFAs or eicosapentaenoic acid (EPA) alone to investigate whether the combination has superior beneficial effects on the outcome of asthmatic mice. Mice were sensitized with house dust mite (HDM) extract, and subsequently supplemented with either a combination of LCPUFAs or EPA alone in a recall asthma model

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Wood, Tyler T., Duane R. Winden, Derek R. Marlor, et al. "Acute secondhand smoke-induced pulmonary inflammation is diminished in RAGE knockout mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 10 (2014): L758—L764. http://dx.doi.org/10.1152/ajplung.00185.2014.

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The receptor for advanced glycation end-products (RAGE) has increasingly been demonstrated to be an important modulator of inflammation in cases of pulmonary disease. Published reports involving tobacco smoke exposure have demonstrated increased expression of RAGE, its participation in proinflammatory signaling, and its role in irreversible pulmonary remodeling. The current research evaluated the in vivo effects of short-term secondhand smoke (SHS) exposure in RAGE knockout and control mice compared with identical animals exposed to room air only. Quantitative PCR, immunoblotting, and immunohi

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Sawafuji, Makoto, Akitoshi Ishizaka, Mitsutomo Kohno, et al. "Role of Rho-kinase in reexpansion pulmonary edema in rabbits." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 6 (2005): L946—L953. http://dx.doi.org/10.1152/ajplung.00188.2004.

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Reexpansion of a collapsed lung increases the microvascular permeability and causes reexpansion pulmonary edema. Neutrophils and their products have been implicated in the development of this phenomenon. The small GTP-binding proteins Rho and its target Rho-kinase (ROCK) regulate endothelial permeability, although their roles in reexpansion pulmonary edema remain unclear. We studied the contribution of ROCK to pulmonary endothelial and epithelial permeability in a rabbit model of this disorder. Endothelial and epithelial permeability was assessed by measuring the tissue-to-plasma (T/P) and bro

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Wilson, Mark S., Satish K. Madala, Thirumalai R. Ramalingam та ін. "Bleomycin and IL-1β–mediated pulmonary fibrosis is IL-17A dependent". Journal of Experimental Medicine 207, № 3 (2010): 535–52. http://dx.doi.org/10.1084/jem.20092121.

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Idiopathic pulmonary fibrosis (IPF) is a destructive inflammatory disease with limited therapeutic options. To better understand the inflammatory responses that precede and concur with collagen deposition, we used three models of pulmonary fibrosis and identify a critical mechanistic role for IL-17A. After exposure to bleomycin (BLM), but not Schistosoma mansoni eggs, IL-17A produced by CD4+ and γδ+ T cells induced significant neutrophilia and pulmonary fibrosis. Studies conducted with C57BL/6 il17a−/− mice confirmed an essential role for IL-17A. Mechanistically, using ifnγ−/−, il10−/−, il10−/

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Tang, W. W., E. S. Yi, D. G. Remick, et al. "Intratracheal injection of endotoxin and cytokines. IX. Contribution of CD11a/ICAM-1 to neutrophil emigration." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 5 (1995): L653—L659. http://dx.doi.org/10.1152/ajplung.1995.269.5.l653.

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Intratracheal injection of endotoxin [lipopolysaccharide (LPS)] in rats causes acute inflammation characterized by the emigration of neutrophils (PMNs) into the bronchoalveolar airspace. Antibody to PMN adhesion molecule CD11a inhibited LPS-initiated PMN accumulation in bronchoalveolar lavage (BAL) fluid by 32% (P < 0.001). Antibody to the endothelial CD11a counterreceptor intercellular adhesion molecule-1 (ICAM-1) inhibited LPS-initiated PMN accumulation in BAL fluid by 66% (P < 0.0001). Combined antibody blockade of ICAM-1 and the C-X-C chemokine cytokine-induced neutrophil chemoattrac

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Gawin, A. Z., J. N. Baraniuk, Y. Igarashi, and M. A. Kaliner. "Effects of capsaicin desensitization on nasal mucosal secretion in guinea pigs in vivo." Journal of Applied Physiology 75, no. 2 (1993): 798–804. http://dx.doi.org/10.1152/jappl.1993.75.2.798.

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Capsaicin-sensitive mechanisms may contribute to histamine's effects on guinea pig nasal mucosal secretion in vivo. Histamine nasal provocations were performed, secretions were collected, and the following variables were measured: total protein (marker of all secretory processes), alkaline phosphatase (marker of glandular secretion), and albumin (marker of vascular permeability, epithelial permeability, and glandular transport). By challenging only one nostril (ipsilateral), the contralateral responses to these challenges were examined and the nature of "nasonasal" reflexes was determined. His

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Widney, Daniel P., Yan Hu, Amy K. Foreman-Wykert, et al. "CXCR3 and Its Ligands Participate in the Host Response to Bordetella bronchiseptica Infection of the Mouse Respiratory Tract but Are Not Required for Clearance of Bacteria from the Lung." Infection and Immunity 73, no. 1 (2005): 485–93. http://dx.doi.org/10.1128/iai.73.1.485-493.2005.

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ABSTRACT Intranasal inoculation of mice with Bordetella bronchiseptica produces a transient pneumonia that is cleared over several weeks in a process known to require both neutrophils and lymphocytes. In this study, we evaluated the roles of the chemokines MIG (CXCL9), IP-10 (CXCL10), and I-TAC (CXCL11) and their common receptor, CXCR3. Following bacterial inoculation, message expression of interleukin-1 (IL-1), IL-6, and the neutrophil-attracting chemokines KC, LIX, and MIP-2 was rapidly induced, with maximal expression found at 6 h. In contrast, message expression of gamma interferon, MIG, I

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Hwang, Hye Suk, Young-Tae Lee, Ki-Hye Kim та ін. "Roles of the Fc Receptor γ-Chain in Inducing Protective Immune Responses after Heterologous Vaccination against Respiratory Syncytial Virus Infection". Vaccines 9, № 3 (2021): 232. http://dx.doi.org/10.3390/vaccines9030232.

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The roles of the Fc receptor (FcR) in protection or inflammatory disease after respiratory syncytial virus (RSV) vaccination and infection remain unknown. Virus-like particles containing RSV fusion proteins (RSV F-VLPs) induce T-helper type 1 antibody responses and protection against RSV. Heterologous RSV F-VLP prime and formalin-inactivated RSV (FI-RSV) boost vaccination has been reported to be effective in providing protection without inflammatory disease. Here, we investigated whether the FcRγ-chain is important for immune protection by the heterologous F-VLP and FI-RSV vaccination using Fc

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Zhang, Sheng, Pengyu Wang, Pengxin Zhao, et al. "Pretreatment of ferulic acid attenuates inflammation and oxidative stress in a rat model of lipopolysaccharide-induced acute respiratory distress syndrome." International Journal of Immunopathology and Pharmacology 31 (January 1, 2018): 039463201775051. http://dx.doi.org/10.1177/0394632017750518.

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Acute respiratory distress syndrome (ARDS) is a fatal clinical condition that can be caused by pulmonary and non-pulmonary diseases. Oxidative stress and inflammation play key roles in the development of ARDS. In this study, we investigated whether ferulic acid (FA), an anti-oxidant, was beneficial for prophylaxis of ARDS. We established an ARDS rat model using lipopolysaccharide (LPS) administration. Lung injury was assessed by lung wet/dry ratio and broncho-alveolar lavage fluid (BALF) analysis. Hematoxylin and eosin staining was performed to evaluate the histological changes of the lungs. E

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