Abstract

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.

Highlights

  • IL-5 has been extensively studied in the context of allergic disease and asthma, due to its critical role in regulating eosinophil biology

  • We demonstrate that IL-5 is required for optimal recovery from influenza A virus (IAV) infection in mice, and that the protective effect of IL-5 is independent of eosinophils, suggesting an alternative cellular target

  • We have previously reported that Group 2 innate lymphoid cell (ILC2) accumulate in the lungs of mice following experimental IAV infection and release large quantities of IL-5 into the bronchoalveolar lavage fluid (BALF), with a parallel increase in eosinophilic inflammation in lungs as would be expected given the well-recognized role of IL5 as an eosinophil chemoattractant and survival factor [16]

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Summary

Introduction

IL-5 has been extensively studied in the context of allergic disease and asthma, due to its critical role in regulating eosinophil biology. Eosinophils, as well as murine B-1 cells, require IL-5 for proliferation, differentiation, and egress out of the bone marrow and into the circulation [1,2,3,4,5,6]. IL-5R is classically thought to be expressed on eosinophils and basophils, but has been reported to be expressed by activated B cells, airway epithelium activated by recombinant. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

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