Exposure to bacterial lipopolysaccharide aggravates H1N1-mediated lung immunopathology via neutrophil extracellular trap formation.

ABSTRACT: Influenza A virus (IAV) is a prevalent pathogen that causes severe respiratory infections worldwide. Currently, the incidence of coinfections between IAV and Gram-negative bacteria has been steadily increasing, and the synergistic interaction between IAV infection and bacterial exposure represents a pivotal risk factor for disease exacerbation. Lipopolysaccharide (LPS), a major Gram-negative bacterial virulence factor, is hypothesized to regulate IAV-induced immune response intensity and disease severity by reshaping the pulmonary immune microenvironment. Here, we established an in vivo coadministration model via intratracheal instillation of low-dose LPS and H1N1 to dissect their synergistic pathogenesis. LPS exposure potentiated H1N1-induced severe lung injury, manifested as persistent n

SUBMITTER: Yan G 

PROVIDER: S-EPMC12627496 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature