IL-10 reduces grain dust-induced airway inflammation and airway hyperreactivity

2000 ◽  
Vol 88 (1) ◽  
pp. 173-179 ◽  
Author(s):  
Timothy J. Quinn ◽  
Somer Taylor ◽  
Christine L. Wohlford-Lenane ◽  
David A. Schwartz
Keyword(s):  
Airway Inflammation ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Interleukin 10 ◽  
Airway Hyperreactivity ◽  
Lower Percentage ◽  
Polymorphonuclear Cells ◽  
Inhalation Challenge ◽  
Grain Dust ◽  
Dust Extract

To determine whether interleukin-10 (IL-10) could alter the development of grain dust-induced airway disease, we pretreated mice with either saline or IL-10 intravenously, exposed the mice to an inhalation challenge with corn dust extract (CDE), and measured inflammation and the development of airway hyperreactivity. Pretreatment with IL-10, in comparison to saline, reduced the concentration and percentage of polymorphonuclear cells in the lavage fluid 30 min after the inhalation challenge with CDE ( P < 0.05). In comparison to saline-treated mice, IL-10 did not significantly alter the degree of airway hyperreactivity 30 min after the exposure to CDE. IL-10-treated mice lavaged 18 h after challenge with CDE also exhibited a lower percentage of polymorphonuclear cells in the lavage fluid ( P < 0.05) and had significantly less airway hyperreactivity than did mice pretreated with the saline placebo ( P < 0.05). These findings indicate that exogenous IL-10 is effective in reducing airway inflammation and airway hyperreactivity due to the inhalation of CDE.

Endotoxin responsiveness and subchronic grain dust-induced airway disease

2001 ◽  
Vol 280 (2) ◽  
pp. L203-L213 ◽  
Author(s):  
Caroline L. S. George ◽  
Hong Jin ◽  
Christine L. Wohlford-Lenane ◽  
Marsha E. O'Neill ◽  
John C. Phipps ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Recovery Period ◽  
Airflow Obstruction ◽  
Airway Disease ◽  
Airway Hyperreactivity ◽  
Lower Airway ◽  
Chronic Airway Disease ◽  
Grain Dust ◽  
Dust Extract ◽  
Chronic Airway

Endotoxin is one of the principal components of grain dust that causes acute reversible airflow obstruction and airway inflammation. To determine whether endotoxin responsiveness influences the development of chronic grain dust-induced airway disease, physiological and airway inflammation remodeling parameters were evaluated after an 8-wk exposure to corn dust extract (CDE) and again after a 4-wk recovery period in a strain of mice sensitive to (C3H/HeBFeJ) and one resistant to (C3H/HeJ) endotoxin. After the CDE exposure, both strains of mice had equal airway hyperreactivity to a methacholine challenge; however, airway hyperreactivity persisted only in the C3H/HeBFeJ mice after the recovery period. Only the C3H/HeBFeJ mice showed significant inflammation of the lower airway after the 8-wk exposure to CDE. After the recovery period, this inflammatory response completely resolved. Lung stereological measurements indicate that an 8-wk exposure to CDE resulted in persistent expansion of the airway submucosal cross-sectional area only in the C3H/HeBFeJ mice. Collagen type III and an influx of cells into the subepithelial area participated in the expansion of the submucosa. Our findings demonstrate that subchronic inhalation of grain dust extract results in the development of chronic airway disease only in mice sensitive to endotoxin but not in mice that are genetically hyporesponsive to endotoxin, suggesting that endotoxin is important in the development of chronic airway disease.

Inhibition of LPS-induced airway hyperresponsiveness and airway inflammation by LPS antagonists

2001 ◽  
Vol 280 (4) ◽  
pp. L771-L778 ◽  
Author(s):  
David A. Schwartz ◽  
William J. Christ ◽  
Steven R. Kleeberger ◽  
Christine L. Wohlford-Lenane
Keyword(s):  
Airway Inflammation ◽  
Intratracheal Instillation ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Airway Hyperreactivity ◽  
Sterile Saline ◽  
Factor Α

To determine whether the inflammatory effects of inhaled endotoxin could be prevented, we pretreated mice with synthetic competitive antagonists (975, 1044, and 1287) for lipopolysaccharide (LPS) before a LPS inhalation challenge. In preliminary studies, we found that these LPS antagonists did not act as agonists in vitro (THP-1 cells) or in vivo (after intratracheal instillation of 10 μg) and that these compounds (at least 1 μg/ml) effectively antagonized the release of tumor necrosis factor-α by LPS-stimulated THP-1 cells. Pretreatment of mice with 10 μg of either 1044 or 1287 resulted in a decrease in the LPS-induced airway hyperreactivity. Moreover, pretreatment of mice with 10 μg of 975, 1044, or 1287 resulted in significant reductions in LPS-induced lung lavage fluid concentrations of total cells, neutrophils, and specific proinflammatory cytokines compared with mice pretreated with sterile saline. Using residual oil fly ash to induce airway inflammation, we found that the action of the LPS antagonists was specific to LPS-induced airway disease. These results suggest that LPS antagonists may be an effective and potentially safe treatment for endotoxin-induced airway disease.

Allergen-induced airway disease is mouse strain dependent

2003 ◽  
Vol 285 (1) ◽  
pp. L32-L42 ◽  
Author(s):  
Gregory S. Whitehead ◽  
Julia K. L. Walker ◽  
Katherine G. Berman ◽  
W. Michael Foster ◽  
David A. Schwartz
Keyword(s):  
Inbred Mouse ◽  
Inbred Strains ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Lung Lavage ◽  
Airway Hyperreactivity ◽  
Mouse Strains ◽  
Airway Eosinophilia ◽  
Biological Responses ◽  
Inbred Strains Of Mice

We investigated the development of airway hyperreactivity (AHR) and inflammation in the lungs of nine genetically diverse inbred strains of mice [129/SvIm, A/J, BALB/cJ, BTBR+(T)/tf/tf, CAST/Ei, C3H/HeJ, C57BL/6J, DBA/2J, and FVB/NJ] after sensitization and challenge with ovalbumin (OVA). At 24, 48, and 72 h post-OVA exposure, the severity of AHR and eosinophilic inflammation of the mouse strains ranged from relatively unresponsive to responsive. The severity of the airway eosinophilia of some strains did not clearly correlate with the development of AHR. The temporal presence of T helper type 2 cytokines in lung lavage fluid also varied markedly among the strains. The levels of IL-4 and IL-13 were generally increased in the strains with the highest airway eosinophilia at 24 and 72 h postexposure, respectively; the levels of IL-5 were significantly increased in most of the strains with airway inflammation over the 72-h time period. The differences of physiological and biological responses among the inbred mouse strains after OVA sensitization and challenge support the hypothesis that genetic factors contribute, in part, to the development of allergen-induced airway disease.

scholarly journals Diabetes Downregulates Allergen-Induced Airway Inflammation in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Vinicius F. Carvalho ◽  
Emiliano O. Barreto ◽  
Ana Carolina S. Arantes ◽  
Magda F. Serra ◽  
Tatiana Paula T. Ferreira ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Bronchoalveolar Lavage Fluid ◽  
Allergic Airway Inflammation ◽  
Allergic Diseases ◽  
Lavage Fluid ◽  
Airway Hyperreactivity ◽  
Eosinophil Infiltration ◽  
Mucus Production ◽  
Diabetes Induction

Previous studies described that allergic diseases, including asthma, occur less often than expected in patients with type 1 diabetes. Here, we investigated the influence of diabetes on allergic airway inflammation in a model of experimental asthma in mice. Diabetes was induced by intravenous injection of alloxan into 12 h-fasted A/J mice, followed by subcutaneous sensitization with ovalbumin (OVA) and aluminum hydroxide (Al(OH)3), on days 5 and 19 after diabetes induction. Animals were intranasally challenged with OVA (25 μg), from day 24 to day 26. Alloxan-induced diabetes significantly attenuated airway inflammation as attested by the lower number of total leukocytes in the bronchoalveolar lavage fluid, mainly neutrophils and eosinophils. Suppression of eosinophil infiltration in the peribronchiolar space and generation of eosinophilotactic mediators, such as CCL-11/eotaxin, CCL-3/MIP-1α, and IL-5, were noted in the lungs of diabetic sensitized mice. In parallel, reduction of airway hyperreactivity (AHR) to methacholine, mucus production, and serum IgE levels was also noted under diabetic conditions. Our findings show that alloxan diabetes caused attenuation of lung allergic inflammatory response in A/J mice, by a mechanism possibly associated with downregulation of IgE antibody production.

scholarly journals VIWITHAN: A STANDARDIZED ASHWAGANDHA EXTRACT AMELIORATES OVALBUMININDUCED AIRWAY-INFLAMMATION AND OXIDATIVE STRESS IN MOUSE MODEL

2021 ◽  
pp. 89-93
Author(s):  
VASAVI HS ◽  
SUDEEP HV ◽  
RAMANAIAH ILLURI ◽  
SHYAMPRASAD K
Keyword(s):  
Oxidative Stress ◽  
Airway Inflammation ◽  
Transforming Growth Factor ◽  
Lavage Fluid ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Lung Pathology ◽  
Protective Effects ◽  
Lung Weight ◽  
And Oxidative Stress

Objective: Withania somnifera, commonly known as Ashwagandha, Indian ginseng, has been used in Ayurvedic and indigenous medicinal preparations for various disease conditions since long time. In the present study, we investigated the protective effects of Viwithan, a standardized proprietary extract from Ashwagandha roots, against airway-inflammation and oxidative stress modulation in an ovalbumin (OVA)-induced murine model of inflammation. Methods: Allergic asthma was initiated in BALB/c mice by sensitizing with OVA on days 1 and 14, followed by intranasal challenge with OVA on days 27, 28, and 29. Mice were administered Viwithan (200 and 400 mg/kg) by oral gavage before challenge. Then, mice were evaluated for the presence of airway inflammation, production of allergen-specific cytokine response, lung pathology, and oxidative stress modulation. Results: The results showed that treatment with Viwithan attenuated OVA-induced lung inflammation in mice. Viwithan significantly attenuated inflammatory cell infiltration into the bronchoalveolar lavage fluid and markedly reduced the levels of pro-inflammatory cytokines, interleukin-10, and transforming growth factor-β1 in lung tissues. Viwithan treatment considerably reduced the lung weight in OVA-sensitized mice. Viwithan markedly attenuated the OVA-induced generation of reactive oxygen species in lung tissues. Conclusion: Together, these results suggested that Viwithan alleviates OVA-induced airway-inflammation and oxidative stress, highlighting the potential of standardized Ashwagandha extract as a useful therapeutic agent for pulmonary fibrosis management.

Relation of Interleukin-10 in Bronchoalveolar Lavage Fluid and Airway Inflammation in Bronchial Asthma

1999 ◽  
Vol 46 (1) ◽  
pp. 44
Author(s):  
Sook Young Lee ◽  
Hung Gue Youn ◽  
Youn Shin ◽  
Sang Haak Lee ◽  
Seok Chan Kim ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Airway Inflammation ◽  
Bronchial Asthma ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Interleukin 10

Montelukast prevents the decrease of interleukin-10 and inhibits NF-κB activation in inflammatory airway of asthmatic guinea pigs

2006 ◽  
Vol 84 (5) ◽  
pp. 531-537 ◽  
Author(s):  
Yuqing Wu ◽  
Chenghua Zhou ◽  
Jin Tao ◽  
Shengnan Li
Keyword(s):  
Airway Inflammation ◽  
Guinea Pigs ◽  
Gradient Centrifugation ◽  
Pulmonary Inflammation ◽  
Lavage Fluid ◽  
Nuclear Factor Κb ◽  
Interleukin 10 ◽  
High Dose ◽  
Model Group ◽  
Asthma Model

Interleukin (IL)-10 is an important immunoregulatory and anti-inflammatory cytokine, whereas nuclear factor-κB (NF-κB) plays an important role in the pathogenesis of asthma. In the present study, the effects of montelukast on the level of IL-10 and on the activation of NF-κB in the inflammatory airway of asthmatic guinea pigs were investigated. Guinea pigs were sensitized by ovalbumin. Pulmonary inflammation was observed by hematoxylin and eosin staining. The eosinophils in broncho-alveolar lavage fluid and blood were separated by density gradient centrifugation and counted under microscope. The level of IL-10 in broncho-alveolar lavage fluid was measured by enzyme-linked immunoadsorbent assay. Activation of NF-κB in lung tissues was inspected by immunohistochemistry. Montelukast at medium and high doses prevented the decrease of IL-10 in broncho-alveolar lavage fluid (n = 8, p < 0.01 vs. asthma model group), inhibited the activation of NF-κB in lung tissues (n = 8; medium dose, p < 0.05; high dose, p < 0.01; vs. asthma model group). There was a significantly negative correlation between the level of IL-10 and the activation of NF-κB in lung tissues (r = –0.488, p < 0.01). Montelukast reduced the severity of airway inflammation and the number of eosinophils in asthmatic guinea pigs. From all these findings we conclude that montelukast can prevent the decrease of IL-10 and inhibit the activation of NF-κB in inflammatory airway of asthmatic guinea pigs, which may be the new important mechanisms of montelukast’s anti-airway-inflammation effects in asthmatic guinea pigs.

scholarly journals Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4+CD25+ regulatory T cells is interleukin 10 dependent

2005 ◽  
Vol 202 (11) ◽  
pp. 1539-1547 ◽  
Author(s):  
Jennifer Kearley ◽  
Jane E. Barker ◽  
Douglas S. Robinson ◽  
Clare M. Lloyd
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Airway Inflammation ◽  
Intracellular Cytokine Staining ◽  
Allergen Challenge ◽  
Interleukin 10 ◽  
Airway Hyperreactivity ◽  
Th2 Cytokine ◽  
Th2 Cell

Deficient suppression of T cell responses to allergen by CD4+CD25+ regulatory T cells has been observed in patients with allergic disease. Our current experiments used a mouse model of airway inflammation to examine the suppressive activity of allergen-specific CD4+CD25+ T cells in vivo. Transfer of ovalbumin (OVA) peptide–specific CD4+CD25+ T cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils, and T helper type 2 (Th2) cytokine expression in the lung after allergen challenge. This suppression was dependent on interleukin (IL) 10 because increased lung expression of IL-10 was detected after transfer of CD4+CD25+ T cells, and regulation was reversed by anti–IL-10R antibody. However, suppression of AHR, airway inflammation, and increased expression of IL-10 were still observed when CD4+CD25+ T cells from IL-10 gene–deficient mice were transferred. Intracellular cytokine staining confirmed that transfer of CD4+CD25+ T cells induced IL-10 expression in recipient CD4+ T cells, but no increase in IL-10 expression was detected in airway macrophages, dendritic cells, or B cells. These data suggest that CD4+CD25+ T cells can suppress the Th2 cell–driven response to allergen in vivo by an IL-10–dependent mechanism but that IL-10 production by the regulatory T cells themselves is not required for such suppression.

scholarly journals Changes in the Secretion of Anti-Inflammatory Cytokines and Acute-Phase Proteins in the Uterus after Artificial Insemination in the Mare

Animals ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 2438
Author(s):  
Katarzyna Wojtysiak ◽  
Wojciech Ryszka ◽  
Tadeusz Stefaniak ◽  
Jarosław Król ◽  
Roland Kozdrowski
Keyword(s):  
Artificial Insemination ◽  
Acute Phase Proteins ◽  
Interleukin 1 ◽  
Lavage Fluid ◽  
Interleukin 10 ◽  
Polymorphonuclear Cells ◽  
Amyloid A ◽  
Before And After ◽  
The Status ◽  
Group 2

The objective of the study was to evaluate the concentrations of interleukin-1 receptor antagonist (IL-1RA), interleukin-10 (IL-10), serum amyloid A (SAA) and haptoglobin (Hp) in uterine lavage fluid before and after artificial insemination (AI). Based on ultrasound examination, mares were divided into: Group 1 (n = 9), no fluid was detected in the uterus during estrus and 7 h after AI; Group 2 (n = 8), no fluid was detected in the uterus during estrus but 7 h after AI fluid was detected in the uterus; Group 3 (n = 8), fluid was detected in the uterus during estrus and also 7 h after AI. In all groups of mares, a significant increase in polymorphonuclear cells (PMN) and a significant increase in IL-1RA and SAA were recorded 7 h after AI. The obtained results show that, regardless of the status of the mare before AI, the endometrial response characterized by PMN influx, and SAA, Hp, IL-1RA and IL-10 production, is similar. The presence of intrauterine fluid during estrus is not connected with PMN influx but can impact uterine IL-1RA production at this time.

scholarly journals Mcl-1 protects eosinophils from apoptosis and exacerbates allergic airway inflammation

Thorax ◽  
2020 ◽  
Vol 75 (7) ◽  
pp. 600-605
Author(s):  
Jennifer M Felton ◽  
David A Dorward ◽  
Jennifer A Cartwright ◽  
Philippe MD Potey ◽  
Calum T Robb ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Kinase Inhibitor ◽  
Allergic Airway Inflammation ◽  
Allergic Diseases ◽  
Airway Disease ◽  
Lavage Fluid ◽  
Allergic Airway Disease ◽  
Cyclin Dependent Kinase ◽  
Mucus Production ◽  
Effector Cells

Eosinophils are key effector cells in allergic diseases. Here we investigated Mcl-1 (an anti-apoptotic protein) in experimental allergic airway inflammation using transgenic overexpressing human Mcl-1 mice (hMcl-1) and reducing Mcl-1 by a cyclin-dependent kinase inhibitor. Overexpression of Mcl-1 exacerbated allergic airway inflammation, with increased bronchoalveolar lavage fluid cellularity, eosinophil numbers and total protein, and an increase in airway mucus production. Eosinophil apoptosis was suppressed by Mcl-1 overexpression, with this resistance to apoptosis attenuated by cyclin-dependent kinase inhibition which also rescued Mcl-1-exacerbated allergic airway inflammation. We propose that targeting Mcl-1 may be beneficial in treatment of allergic airway disease.

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