CLEC5A-Mediated Enhancement of the Inflammatory Response in Myeloid Cells Contributes to Influenza Virus Pathogenicity In Vivo.
Ooiean TengSzu-Ting ChenTsui-Ling HsuSin Fun SiaSuzanne ColeSophie A ValkenburgTzu-Yun HsuJian Teddy ZhengWenwei TuRoberto BruzzoneJoseph Sriyal Malik PeirisShie-Liang HsiehHui Ling YenPublished in: Journal of virology (2016)
Multiple pattern recognition receptors work in synergy to sense viral RNA or proteins synthesized during influenza replication and mediate host responses for viral control. Well-orchestrated host responses may help to maintain the inflammatory response to minimize tissue damage while inducing an effective adaptive immune response for viral clearance. We identified that CLEC5A, a C-type lectin receptor which has previously been reported to mediate flavivirus-induced inflammatory responses, enhanced induction of proinflammatory cytokines and chemokines in myeloid cells after influenza infections. CLEC5A-deficient mice infected with influenza virus showed reduced inflammation in the lungs and improved survival compared to that of the wild-type mice despite comparable viral loads. The survival difference was more prominent at a lower dose of inoculum. Collectively, our results suggest that dampening CLEC5A-mediated inflammatory responses in myeloid cells reduces immunopathogenesis after influenza infections.
Keyphrases
- induced apoptosis
- sars cov
- oxidative stress
- cell cycle arrest
- inflammatory response
- immune response
- dendritic cells
- wild type
- bone marrow
- acute myeloid leukemia
- endoplasmic reticulum stress
- escherichia coli
- metabolic syndrome
- staphylococcus aureus
- adipose tissue
- cystic fibrosis
- cell death
- insulin resistance
- toll like receptor
- lps induced
- high glucose
- drug induced