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Updated: Jan 6, 2026

A Non-invasive and Technically Non-intensive Method for Induction and Phenotyping of Experimental Bacterial Pneumonia in Mice
Published on: September 28, 2016
Bacterial Pneumonia Alters the Respiratory Microbiota and Inflammatory Profile Via the Lung Microbiome-Immune Axis
Xiaoyi Ye1, Binghan Shen2, Zhiming Cai2
1Department of Respiratory and Critical Care Medicine, Quanzhou First Hospital Affiliated to Fujian Medical University, 252# East Street, Licheng District, Quanzhou, 362000, Fujian, China. y2841966370@163.com.
Abstract:
Bacterial invasion of the lungs causes pneumonia, which poses a serious threat to public health. In the absence of pathogen identification, the misuse of antibacterial agents contributes to bacterial resistance. This study investigated changes in the respiratory microbiome and proinflammatory profiles in bronchoalveolar lavage fluid (BALF) from patients with bacterial pneumonia before and after treatment, compared with healthy controls. Leukocyte count, granulocyte count, and neutrophil percentage were significantly elevated in patients with bacterial pneumonia. Microbial species richness in the untreated pneumonia group (group A) was significantly lower than in the treated group (group B) and healthy controls (group C). Significant differences in α-diversity and β-diversity were observed across all three groups. Linear discriminant analysis effect size (LEfSe) identified 19 microbial biomarkers at the genus level. Levels of TNF-α and IL-6 in BALF and serum were significantly reduced in group A following treatment, as measured by ELISA. Correlation analysis revealed associations between proinflammatory cytokines and several genera, including P5D1_392, Chloroplast, Blautia, Flavonifractor, Terrisporobacter, [Ruminococcus]_gauvreauii_group, Anaerostipes, Ruminococcus, Parabacteroides, Ellin6055, and Clostridia_UCG-014. These findings suggest that bacterial pneumonia disrupts the respiratory microbiota and alters the inflammatory profile through the lung microbiome-immune axis, leading to immune dysregulation. This work provides a theoretical basis for targeted treatment strategies in bacterial pneumonia.
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