ArticleFrontiers in microbiology2021
Interleukin 16 Enhances the Host Susceptibility to Influenza A Virus Infection.
Article in Frontiers in microbiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- PARP12-mediated mono-ADP-ribosylation as a checkpoint for necroptosis and apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Pulmonary adaptation to repeated poly(I:C) exposure is impaired in asthmatic mice: an observational study.Respiratory research · 2024Article
- An eQTL-based approach reveals candidate regulators of LINE-1 RNA levels in lymphoblastoid cells.PLoS genetics · 2024Article
- Mechanisms of ammonotelism, epithelium damage, cellular apoptosis, and proliferation in gill of Litopenaeus vannamei under NHEnvironmental science and pollution research international · 2024Article
- An eQTL-based Approach Reveals Candidate Regulators of LINE-1 RNA Levels in Lymphoblastoid Cells.bioRxiv : the preprint server for biology · 2023Article
- Identification of Host PDZ-Based Interactions with the SARS-CoV-2 E Protein in Human Monocytes.International journal of molecular sciences · 2023Article
- A decline in avian cytokine expression with age revealed by commercially available cytokine array.Frontiers in physiology · 2023Article
- Interleukin (IL) 16: a candidate urinary biomarker for proliferative lupus nephritis.Lupus science & medicine · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Influenza A virus (IAV) is a major respiratory pathogen that causes seasonal and pandemic flu, being a threat to global health. Various viral and cellular factors have been characterized to support or limit IAV infection. Interleukin 16 (IL16) has been known as one of the blood signature biomarkers discriminating systemic inflammation due to viral infection vs. other etiologies. Here, we report that the level of IL16 was elevated in the serum samples, lung homogenates, and bronchoalveolar lavage fluid of IAV-infected mice. IL16 overexpression facilitated IAV replication. Conversely, loss of IL16 reduced the host susceptibility to IAV infection
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