Although there is increasing evidence that IL-17 is involved in protective immunity against H1 and H3 influenza virus infections, little is known about the role of IL-17 in the highly pathogenic H5N1 influenza virus infection.
Because IL-17A and IL-17F, ligands for IL-17 receptor antagonist (IL-17RA), have been shown to mediate neutrophil migration into the lung in response to LPS or Gram-negative bacterial pneumonia, we hypothesized that IL-17RA signaling was critical for acute lung injury in response to pulmonary influenza infection.
By conducting the MCCV on seed cross-talk, 3 hub cross-talk for BPD were uncovered: i) The pair of pathways role of interleukin-17F (IL-17F) in allergic inflammatory airway diseases and role of IL-17A in psoriasis; ii) the pair of pathways role of IL random forest 17A in psoriasis and IL-17A signaling in fibroblasts and ii) the pair of pathways IL-17A signaling in airway cells and role of hypercytokinemia/hyperchemokinemia in the pathogenesis of influenza.
Our data show that although IL-17A reduces S. pneumoniae colonization, coinfection with influenza virus elicits a robust innate IL-17A response that promotes inflammation and S. pneumoniae disease in the nasopharynx.
The frequencies of the IL-1β rs16944 (P = 0.007) and IL-17rs2275913 (P = 0.006) genotypes were associated with severe influenza disease, while the frequencies of IL-10 rs1800872 and IL-28 rs8099917 were not associated with the disease (P > 0.05).