The IL-17A-neutrophil axis promotes epithelial cell IL-33 production during nematode lung migration

Jesuthas Ajendra (Lead / Corresponding author), Pedro H. Papotto, James E. Parkinson, Rebecca J. Dodd, André L. Bombeiro, Stella Pearson, Brian H. K. Chan, Julie C. Ribot, Henry J. McSorley, Tara E. Sutherland, Judith E. Allen (Lead / Corresponding author)

Research output: Contribution to journalArticlepeer-review

7 Downloads (Pure)

Abstract

The early migratory phase of pulmonary helminth infections is characterized by tissue injury leading to the release of the alarmin interleukin (IL)-33 and subsequent induction of type 2 immune responses. We recently described a role for IL-17A, through suppression of interferon (IFN)-γ, as an important inducer of type 2 responses during infection with the lung-migrating rodent nematode Nippostrongylus brasiliensis. Here, we aimed to investigate the interaction between IL-17A and IL-33 during the early lung migratory stages of N. brasiliensis infection. In this brief report, we demonstrate that deficiency of IL-17A leads to impaired IL-33 expression and secretion early in infection, independent of IL-17A suppression of IFN-γ. Neutrophil-depletion experiments, which dramatically reduce lung injury, revealed that neutrophils are primarily responsible for the IL-17A-dependent release of IL-33 into the airways. Taken together, our results reveal an IL-17A-neutrophil-axis that can drive IL-33 during helminth infection, highlighting an additional pathway by which IL-17A regulates pulmonary type 2 immunity.

Original languageEnglish
Pages (from-to)767-775
Number of pages9
JournalMucosal Immunology
Volume16
Issue number6
Early online date30 Sept 2023
DOIs
Publication statusPublished - Dec 2023

Fingerprint

Dive into the research topics of 'The IL-17A-neutrophil axis promotes epithelial cell IL-33 production during nematode lung migration'. Together they form a unique fingerprint.

Cite this