Abstract

Background Infantile pneumonia is a common health concern worldwide, with elevated morbidity and mortality rates among affected children. This study aims to identify key genes associated with infantile pneumonia using bioinformatics and unravel the underlying mechanisms. Results OLFM4 was the only biomarker identified for infantile pneumonia. Besides, OLFM4 expression was promoted in the serum of infantile pneumonia patients, and LPS-stimulated cells and mice models. OLFM4 knockdown repressed cell apoptosis, levels of TNF-α, IL-6, IL-1β, MPO, MDA, ROS, and activation of the NF-κB pathway, and facilitated the SOD level of LPS-induced models. OLFM4 knockdown alleviated the lung injury of the LPS-induced mouse model. Conclusions OLFM4 knockdown alleviated cell apoptosis, inflammatory response, and oxidative stress via the NF-κB signaling pathway in LPS-induced WI-38 cells and mice model. The findings suggest that OLFM4 may pave the way for the treatment of infantile pneumonia.