Gut microbiota-derived α-linoleic acid mitigates intestinal inflammation induced by oral infection with Toxoplasma gondii
Toxoplasma gondii (T. gondii) can cause serious zoonotic disease. Oral infection of cysts is the main transmission route of T. gondii and there is a lack of safe and effective anti-T. gondii drugs. It has been reported that T. gondii can significantly alter the structure and metabolism of gut microbiota, thereby affecting the process of T. gondii infection. Probiotics have been shown to be effective in the treatment of T. gondii infection; however, there is still limited systematic research on the action and mechanism of gut microbiota and its metabolites that regulate intestinal inflammation caused by T. gondii infection. In our previous study, it was found that α-AMY gene is essential for maintaining chronic infection, and the virulence between α-AMY knockout and wild-type cysts was significantly different. Based on the α-AMY knockout cyst, we proposed a scientific hypothesis that the severity of T. gondii infection in different strains is closely related to the gut microbiota from the perspective of the interaction between gut microbiota and T. gondii infection. This project intends to analyze and identify the key gut microbiota and metabolites that affect the process of T. gondii infection using a multi-omics approach combining 16S rRNA sequencing and metabolomics, and to further elucidate the mechanism of action of gut microbiota and their metabolites in regulating intestinal inflammation caused by T. gondii infection through the TLR4/MyD88/NF-κB pathway, which will provide important guiding significance for the development of drugs to treat toxoplasmosis.