Parasite immunology · 2020
Intestinal microbiota regulates tryptophan metabolism following oral infection with Toxoplasma gondii.
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Dos Santos Liliane M, Commodaro Alessandra G, Vasquez Alicia R R, Kohlhoff Markus, de Paula Guerra Daniel A, Coimbra Roney S, Martins-Filho Olindo A, Teixeira-Carvalho Andrea, Rizzo Luiz V, Vieira Leda Q, Serra Horacio M
Аннотация
INTRODUCTION: The intestinal microbiota plays an important role in modulating host immune responses. Oral Toxoplasma gondii infection can promote intestinal inflammation in certain mice strains. The IDO-AhR axis may control tryptophan (Trp) metabolism constituting an important immune regulatory mechanism in inflammatory settings.
AIMS: In the present study, we investigated the role of the intestinal microbiota on Trp metabolism during oral infection with T gondii.
METHODS AND RESULTS: Mice were treated with antibiotics for four weeks and then infected with T gondii by gavage. Histopathology and immune responses were evaluated 8 days after infection. We found that depletion of intestinal microbiota by antibiotics contributed to resistance against T gondii infection and led to reduced expression of AhR on dendritic and Treg cells. Mice depleted of Gram-negative bacteria presented higher levels of systemic Trp, downregulation of AhR expression and increased resistance to infection whereas depletion of Gram-positive bacteria did not affect susceptibility or expression of AhR on immune cells.
CONCLUSION: Our findings indicate that the intestinal microbiota can control Trp availability and provide a link between the AhR pathway and host-microbiota interaction in acute infection with T gondii.
AIMS: In the present study, we investigated the role of the intestinal microbiota on Trp metabolism during oral infection with T gondii.
METHODS AND RESULTS: Mice were treated with antibiotics for four weeks and then infected with T gondii by gavage. Histopathology and immune responses were evaluated 8 days after infection. We found that depletion of intestinal microbiota by antibiotics contributed to resistance against T gondii infection and led to reduced expression of AhR on dendritic and Treg cells. Mice depleted of Gram-negative bacteria presented higher levels of systemic Trp, downregulation of AhR expression and increased resistance to infection whereas depletion of Gram-positive bacteria did not affect susceptibility or expression of AhR on immune cells.
CONCLUSION: Our findings indicate that the intestinal microbiota can control Trp availability and provide a link between the AhR pathway and host-microbiota interaction in acute infection with T gondii.