Alveolar fibroblasts respond to pseudomonas aeruginosa infection with cytokine secretion: Role in acute lung inflammation

Alveolar fibroblasts play a key role in regulation of lung inflammation. Pseudomonas aeruginosa (PAO) is one of the most common pathogens causing lung injury, and the role of PAO-infected alveolar fibroblasts in such a condition remain unclear. Tumor necrosis factor (TNF)-α was significantly upregulated in alveolar fibroblasts with PAO-associated lung injury patients. Alveolar fibroblasts infected with PAO, combined with gene expression profiling, revealed elevated levels of pro-inflammatory cytokines, and this finding was closely linked to neutrophil-mediated inflammatory injury. Gene Ontology and Kyoto Encyclopedia of Genes Genomes enrichment analysis indicated that differentially expressed genes were linked to pro-inflammatory signals, including necroptosis, nuclear factor (NF)-κB inflammatory signaling, pro-inflammatory cytokine production, and neutrophil migration/activation. Furthermore, Western blot and enzyme-linked immunosorbent assay results demonstrate that PAO activated the NF-κB pathway and enhanced the expression and secretion of pro-inflammatory cytokines in alveolar fibroblasts. The study findings suggest that PAO-infected alveolar fibroblasts contribute to the development of pulmonary inflammatory injury.