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ABSTRACT: Background
Hypercapnic acidosis (HCA) is a hallmark of acute hypercapnic respiratory failure, often triggered by respiratory infections. Its role in lung injury remains controversial, with both protective and detrimental effects reported. However, the specific impact on pulmonary immune responses to lung infections remain poorly understood. To investigate the impact of HCA on alveolar response during infection, we developed an in vitro model combining human alveolar epithelial cells (type I and II) and macrophage-like THP-1 cells.Methods
The co-culture and monocultures were infected with Pseudomonas aeruginosa or Streptococcus pneumoniae under normocapnic or HCA conditions. At 1 hour and 24 hours post-infection, we assessed inflammatory cytokine express
SUBMITTER: Campana-Duel E
PROVIDER: S-EPMC12909561 | biostudies-literature | 2025
REPOSITORIES: biostudies-literature