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Objective To investigate the effect of Lactobacillus acidophilus (L. acidophilus) on the inflammation of mice with lipopolysaccharide (LPS)-induced acute pneumonia and the possible mechanism. Methods Twenty-one mice were divided into a control group (NC, n=6), a model group (LPS, n=8) and a L. acidophilus-treated group (Probiotics, n=7). The mice in the control group were fed normally, while those in the LPS and Probiotics groups were treated with 10 mg/kg LPS through tracheal drip to establish a mouse model of acute pneumonia, and those in the Probiotics group were given L. acidophilus. All of the mice were executed in 7 d after modeling. The pathological changes of lung tissue were assessed by HE staining and wet/dry ratio (W/D) of lung tissue. ELISA was used to detect the levels of inflammatory factors in bronchoalveolar lavage fluid and the activity of myeloperoxidase (MPO) in lung tissue. 16S rDNA sequencing was employed to observe the diversity of intestinal flora, and immunohistochemical (IHC) staining was applied to determine the expression of ZO-1 and TRPV4. Results The Probiotics group had significantly reduced W/D ratio and IL-1β, TNF-α and IL-6 levels, increased IL-10 level (P < 0.05), diminished MPO activity (P < 0.05), down-regulated TRPV4 expression in colon and lung tissues, and upregulated ZO-1 expression in colon tissue, meanwhile, the abundance of Helicobacter spp. and Desulfovibrio spp. was significantly altered when compared with the LPS group. Conclusion L. acidophilus alleviates lung inflammation in LPS-induced pneumonia in mice, which may be associated with intestinal abundance of Desulfovibrio spp. in the, activity of TRPV4 channel and intestinal mucosal permeability. |
