Expression of IL-5 receptor alpha by murine and human lung neutrophils

The role of eosinophilia in atopic diseases, including asthma, is well established, as is the well-known role of IL-5 as a major eosinophilopoeitin and chemoattractant. Following influenza A virus infection of mice, type 2 innate lymphoid cells are recruited to the respiratory tract and produce larg...

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Published inPloS one Vol. 14; no. 8; p. e0221113
Main Authors Gorski, Stacey A, Lawrence, Monica G, Hinkelman, Amy, Spano, MarthaJoy M, Steinke, John W, Borish, Larry, Teague, W Gerald, Braciale, Thomas J
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 15.08.2019
Public Library of Science (PLoS)
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Summary:The role of eosinophilia in atopic diseases, including asthma, is well established, as is the well-known role of IL-5 as a major eosinophilopoeitin and chemoattractant. Following influenza A virus infection of mice, type 2 innate lymphoid cells are recruited to the respiratory tract and produce large quantities of IL-5, which contributes to the recruitment of eosinophils into the infected lungs during the recovery phase of infection. We demonstrate here that while IL-5 is required for optimal recovery from influenza A virus infection in BALB/c and C57BL/6 mice, the protective effect of IL-5 is independent of eosinophils, suggesting an alternative cellular target. We describe the unexpected finding of IL-5 receptor alpha (CD125) expression on neutrophils infiltrating the inflamed mouse lungs, as well as on neutrophils at other anatomic sites. We extend this finding of neutrophil CD125 expression to humans, specifically to neutrophils found in the bronchoalveolar lavage fluid from the inflamed lungs of children with treatment-refractory asthma. We further demonstrate that the IL-5 receptor on neutrophils is capable of signal transduction. Our data provide further evidence that neutrophils can play a role bridging atopic type 2 and innate anti-microbial immunity.
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Competing Interests: WGT, LB, JS and TJB receive research funding from Astra Zeneca. LB receives consulting funding from Astra Zeneca and Teva Pharmaceuticals. WGT receives research funding from Teva Pharmaceutic Industries. SG is currently employed by Sanofi Pasteur. There are no patents, products in development or marketed products to declare. This does not alter our adherence to all the PLOS ONE policies on sharing data and materials.
Current address: Sanofi Pasteur, Charlottesville, VA, United States of America
Current address: Department of Microbiology & Immunology, Campbell University, Buies Creek, NC, United States of America
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0221113