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Intestinal Inflammation-Mediated Clearance of Amebic Parasites Is Dependent on IFN-γ

Authors :
Mihoko Kikuchi
Hajime Hisaeda
Shinjiro Hamano
Masachika Senba
Seiji Obi
Chikako Shimokawa
Alex Olia
Seiki Kobayashi
Source :
The Journal of Immunology. 200:1101-1109
Publication Year :
2018
Publisher :
The American Association of Immunologists, 2018.

Abstract

Intestinal amebiasis is a major cause of diarrhea. However, research on host–amebae interactions has been hampered owing to a lack of appropriate animal models. Recently, a mouse model of intestinal amebiasis was established, and using it, we reported that Entamoeba moshkovskii colonized the intestine in a manner similar to that of the pathogenic Entamoeba histolytica. In this study, we evaluated the protective mechanisms present against amebae using this model. CBA/J mice infected with E. histolytica had a persistent infection without apparent symptoms. In contrast, E. moshkovskii–infected mice rapidly expelled the ameba, which was associated with weight loss, diarrhea, and intestinal damage characterized by apoptosis of intestinal epithelial cells (IECs). Expression of NKG2D on intestinal intraepithelial lymphocytes (IELs) and IFN-γ–producing cells in Peyer’s patches were significantly induced after infection with E. moshkovskii but not with E. histolytica. IFN-γ–deficient mice infected with E. moshkovskii showed no obvious symptoms. Notably, none of these mice expelled E. moshkovskii, indicating that IFN-γ is responsible not only for intestinal symptoms but also for the expulsion of amebae. Furthermore, apoptosis of IECs and expression of NKG2D on IELs observed in E. moshkovskii–infected mice did not occur in the absence of IFN-γ. In vivo blocking of NKG2D in mice infected with E. moshkovskii enabled ameba to survive longer and remarkably reduced apoptotic IECs. Our results clearly demonstrate a novel protective mechanism exerted by IFN-γ against intestinal amebae, including induction of cytotoxicity of IELs toward IECs.

Details

ISSN :
15506606 and 00221767
Volume :
200
Database :
OpenAIRE
Journal :
The Journal of Immunology
Accession number :
edsair.doi.dedup.....9402d7a934bd77e5b20758dfc0f0e594
Full Text :
https://doi.org/10.4049/jimmunol.1700806