ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023
DUOX2 regulates secreted factors in virus-infected respiratory epithelial cells that contribute to neutrophil attraction and activation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Germline determinants of toxicity and efficacy in patients with large B-cell lymphoma treated with CAR T-cell therapy.Journal for immunotherapy of cancer · 2025Article
- Construction of a feature gene and machine prediction model for inflammatory bowel disease based on multichip joint analysis.Journal of translational medicine · 2025Article
- No Evidence of Direct Activation of Human Neutrophil Responses by Multivalent Prefusion Trimeric SARS-CoV-2 Spike ProteinbioRxiv : the preprint server for biology · 2025Article
- Transcriptional profiling identification of inflammatory signaling pathways in ulcerative colitis.PloS one · 2025Article
- No evidence of direct activation of human neutrophil responses by multivalent prefusion trimeric SARS-CoV-2 Spike protein ex vivo.PloS one · 2025Article
- DUOX2 regulates secreted factors in virus-infected respiratory epithelial cells that contribute to neutrophil attraction and activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
The first line of defense against respiratory viruses relies on the antiviral and proinflammatory cytokine response initiated in infected respiratory epithelial cells. The cytokine response not only restricts virus replication and spreading, but also orchestrates the subsequent immune response. The epithelial Dual Oxidase 2 (DUOX2) has recently emerged as a regulator of the interferon antiviral response. Here, we investigated the role of DUOX2 in the inflammatory cytokine response using a model of A549 cells deficient in DUOX2 generated using Crispr-Cas9 and infected by Sendai virus. We found that the absence of DUOX2 selectively reduced the induction of a restricted panel of 14 cytokines and chemokines secreted in response to Sendai virus by 20 to 89%. The secreted factors produced by epithelial cells upon virus infection promoted the migration, adhesion, and degranulation of primary human neutrophils, in part through the DUOX2-dependent secretion of TNF and chemokines. In contrast, DUOX2 expression did not impact neutrophil viability or NETosis, thereby highlighting a selective impact of DUOX2 in neutrophil functions. Overall, this study unveils previously unrecognized roles of epithelial DUOX2 in the epithelial-immune cells crosstalk during respiratory virus infection.
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