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

• Published in: PloS one 2019-08, Vol.14 (8), p.e0221113-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: Article
• Language: English
• Subjects: Allergies; Alveoli; Animals; Asthma; Atopy; B cells; Biology and Life Sciences; Bronchus; Care and treatment; Cellular signal transduction; Child; Child, Preschool; Childhood asthma; Cytokine receptors; Cytokines; Development and progression; EDTA; Eosinophilia; Eosinophils; Experiments; Gene expression; Gene Expression Regulation - immunology; Health aspects; House mouse; Humans; Immunity; Immunity, Innate; Immunology; Infection; Infections; Inflammation; Inflammation - immunology; Inflammation - pathology; Influenza; Influenza A; Influenza A virus - immunology; Influenza, Human - immunology; Influenza, Human - pathology; Interleukin 5; Interleukin-5 Receptor alpha Subunit - immunology; Laboratory animals; Leukocytes (eosinophilic); Leukocytes (neutrophilic); Lung - immunology; Lung - pathology; Lungs; Lymphoid cells; Medical research; Medicine; Medicine and Health Sciences; Mice; Mice, Inbred BALB C; Microorganisms; Neutrophils; Neutrophils - immunology; Neutrophils - pathology; Pediatrics; Recovery; Respiratory tract; Th2 Cells - immunology; Th2 Cells - pathology; Transduction; Viruses
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0221113

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.