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Mucosal Immunol. 2018 Jul;11(4):1181-1190. doi: 10.1038/s41385-018-0005-8. Epub 2018 May 4.

Interleukin-22-deficiency and microbiota contribute to the exacerbation of Toxoplasma gondii-induced intestinal inflammation.

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Laboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), CNRS and University of Orleans (UMR7355), Orléans, France.
CNRS UPS44 -TAAM, Orléans, France.
Sorbonne Universités, UPMC Univ. Paris 06, École Normale Supérieure, PSL Research University, CNRS, INSERM, APHP, Laboratoire des Biomolécules (LBM), 27 rue de Chaligny, 75005, Paris, France.
Ludwig Institute for Cancer Research, Université Catholique de Louvain, Brussels, Belgium.
INSERM U1068, Centre de Recherche en Cancérologie de Marseille (CRCM), Aix-Marseille Université and Institut Paoli-Calmette, Parc Scientifique et Technologique de Luminy, CNRS UMR 7258, Marseille, France.
Medizinische Klinik und Poliklinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, 20246, Germany.
L'Institut de Pasteur, Lille, France.
Micalis Institute, Institut National de la Recherche Agronomique (INRA), AgroParisTech, Université Paris-Saclay, Jouy-en-Josas, 78352, France.
Department of Gastroenterology, Saint Antoine Hospital, Assistance Publique-Hopitaux de Paris, UPMC, Paris, France.
Laboratory of Experimental and Molecular Immunology and Neurogenetics (INEM), CNRS and University of Orleans (UMR7355), Orléans, France.


Upon oral infection with Toxoplasma gondii cysts (76 K strain) tachyzoites are released into the intestinal lumen and cross the epithelial barrier causing damage and acute intestinal inflammation in C57BL/6 (B6) mice. Here we investigated the role of microbiota and IL-22 in T.gondii-induced small intestinal inflammation. Oral T.gondii infection in B6 mice causes inflammation with IFNγ and IL-22 production. In IL-22-deficient mice, T.gondii infection augments the Th1 driven inflammation. Deficiency in either IL-22bp, the soluble IL-22 receptor or Reg3γ, an IL-22-dependent antimicrobial lectin/peptide, did not reduce inflammation. Under germ-free conditions, T.gondii-induced inflammation was reduced in correlation with parasite load. But intestinal inflammation is still present in germ-free mice, at low level, in the lamina propria, independently of IL-22 expression. Exacerbated intestinal inflammation driven by absence of IL-22 appears to be independent of IL-22 deficiency associated-dysbiosis as similar inflammation was observed after fecal transplantation of IL-22-/- or WT microbiota to germ-free-WT mice. Our results suggest cooperation between parasite and intestinal microbiota in small intestine inflammation development and endogenous IL-22 seems to exert a protective role independently of its effect on the microbiota. In conclusion, IL-22 participates in T.gondii induced acute small intestinal inflammation independently of microbiota and Reg3γ.

[Indexed for MEDLINE]

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