Baicalin is a plant-derived
flavonoid from Scutellaria baicalensis Georgi with multiple bioactivities and has a protective effect against avian pathogenic Escherichia coli (APEC)
infection. However, the underlying mechanism of
baicalin against APEC
infection is still unknown. Therefore, we aimed to explore whether the protective effects and mechanisms of
baicalin on APEC-induced
lung inflammation were related to the regulation of gut microbiota. The results showed that
baicalin significantly reduced APEC colonization and pro-inflammatory
cytokines production, and additionally recovered air-blood barrier integrity in the lungs after APEC challenge. However, depletion of gut microbiota significantly weakened the protective effects of
baicalin against APEC
infection as mentioned above. Furthermore,
baicalin markedly restored the
dysbiosis of gut microbiota induced by APEC as well as increased the abundance of
short chain fatty acid (SCFA)-producing bacteria and the production of SCFAs including
acetic acid,
propionic acid and
butyric acid, especially
acetic acid. In addition, the concentrations of
acetic acid and its receptor
free fatty acid receptor 2 (FFAR2) were significantly upregulated in the lung tissues after
baicalin treatment. In conclusion, gut microbiota played a key role in the pharmacological action of
baicalin against APEC-induced
lung inflammation.
Baicalin remodeled the
dysbiosis of gut microbiota caused by APEC and increased the production of SCFAs, especially
acetic acid in the gut, and then the increased
acetate may circulate to the lungs to activate FFAR2 to defend APEC
infection. Together, our study suggested that
baicalin inhibited APEC
infection through remodeling the gut microbiota
dysbiosis and increasing the SCFA production. Furthermore,
baicalin may serve as an alternative
antibiotic and a novel therapeutic
drug to prevent or treat APEC
infection.