Abstract
The gastrointestinal tract is a major portal of entry for many pathogens, including the protozoan parasite Toxoplasma gondii. Billions of people worldwide have acquired T. gondii at some point in their life, and for the vast majority this has led to latent infection in the central nervous system. The first line of host defense against Toxoplasma is located within the intestinal mucosa. Appropriate coordination of responses by the intestinal epithelium, intraepithelial lymphocytes, and lamina propria cells results in an inflammatory response that controls acute infection. Under some conditions, infection elicits bacterial dysbiosis and immune-mediated tissue damage in the intestine. Here, we discuss the complex interactions between the microbiota, the epithelium, as well as innate and adaptive immune cells in the intestinal mucosa that induce protective immunity, and that sometimes switch to inflammatory pathology as T. gondii encounters tissues of the gut.
Highlights
Appropriate coordination of responses by the intestinal epithelium, intraepithelial lymphocytes, and lamina propria cells results in an inflammatory response that controls acute infection
We discuss the complex interactions between the microbiota, the epithelium, as well as innate and adaptive immune cells in the intestinal mucosa that induce protective immunity, and that sometimes switch to inflammatory pathology as T. gondii encounters tissues of the gut
These studies describe new, important roles for Paneth cell autophagy and antimicrobial peptide production in limiting immunopathology and microbiota dysbiosis driven by T. gondii infection
Summary
Toxoplasma gondii is a globally distributed microorganism whose host range includes humans, domestic animals, and wildlife. The parasites disseminate through the host as tachyzoites, infecting and proliferating in numerous cell types This is followed by chronic, or latent infection, which is associated with formation of cysts containing the bradyzoite parasite form in muscle tissue and the central nervous system. The reason for this selectivity was a mystery until recently It appears that unique aspects of lipid metabolism in cats results in unusually high systemic levels of linoleic acid that somehow signals parasite gametogenesis (Martorelli Di Genova et al, 2019). This is due to lack of intestinal delta-6-desaturase activity that is required for linoleic acid metabolism. Ingestion of oocysts (the environmentally resistant products of Toxoplasma sexual reproduction) shed in cat feces, as well as direct carnivorism of cysts within muscle tissue helps account for the widespread distribution of T. gondii
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