Abstract
Pneumonia is a severe lower respiratory tract infection. This study demonstrates that phospholipase A2 (PLA2), a potential biomarker for pneumonia, contributes to alveoli damage by hydrolyzing pulmonary surfactant phospholipids. This process impairs gas exchange and generates hemolytic phospholipids that disrupt cellular membranes, exacerbating pulmonary injury. Experimental evidence demonstrates that PLA2 inhibitors significantly alleviate cellular damage in lipopolysaccharide (LPS)-induced pulmonary inflammation. These findings reveal a key mechanistic role of PLA2 in pneumonia pathogenesis and suggest novel therapeutic strategies. The results may provide more effective clinical interventions and guide further research in related fields.