The mechanism of baicalin in improving pulmonary inflammatory response and injury and regulating intestinal flora in Mycoplasma pneumoniae pneumonia mice

Objective

Mycoplasma pneumoniae (MP) is a common pathogen that can cause respiratory infections. We explored the mechanisms of baicalin (BIA) affecting pulmonary inflammation and injury and regulated their intestinal flora through the TLR4/NF-κB pathway in MP pneumonia (MPP) mice with intestinal dysbiosis.

Methods

The intestinal dysbiosis and the MPP mouse models with intestinal dysbiosis were established and treated with different doses of BIA, with lung wet-to-dry weight (W/D) ratio weighed. Kits were conducted to detect MP expression and serum C-reactive protein (CRP)/INF-γ/TNF-α/IL-1β/IL-8 levels, and RT-qPCR and Western blot to determine TLR4/MyD88/NF-κBp65 levels. Lung injury was assessed using HE staining, and intestinal flora structure using 16S rDNA sequencing. Gas chromatography-mass spectrometry determined fecal short-chain fatty acid (SFCA) content.

Results

The broad-spectrum antibiotic mixture caused enlarged cecum, increased contents, darker color, weight loss, decreased intestinal flora abundance and diversity, and intestinal flora structure imbalance in mice. The MP-infected intestinal dysbiosis mice exhibited elevated MP expression, reduced body weight, increased W/D ratio, elevated serum CRP/INF-γ/TNFα/IL-1β/IL-8 levels, as well as interstitial pneumonitis in lungs. TLR4/MyD88/NF-κB p65 were elevated in lung tissues of MPP mice with intestinal dysbiosis. BIA partially reversed pulmonary inflammation and injury, and restored the flora diversity and SCFAs in MPP mice with intestinal dysbiosis.

Conclusion

BIA attenuated pulmonary inflammation and injury and modulated their intestinal flora imbalance by inhibiting the TLR4/NF-κB pathway in MPP mice with intestinal dysbiosis.