RGD Reference Report - Intestinal Inflammation-Mediated Clearance of Amebic Parasites Is Dependent on IFN-γ. - Rat Genome Database

Send us a Message

Submit Data |  Help |  Video Tutorials |  News |  Publications |  Download |  REST API |  Citing RGD |  Contact   

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

Authors: Shimokawa, Chikako  Senba, Masachika  Kobayashi, Seiki  Kikuchi, Mihoko  Obi, Seiji  Olia, Alex  Hamano, Shinjiro  Hisaeda, Hajime 
Citation: Shimokawa C, etal., J Immunol. 2018 Feb 1;200(3):1101-1109. doi: 10.4049/jimmunol.1700806. Epub 2017 Dec 18.
RGD ID: 14975099
Pubmed: PMID:29255076   (View Abstract at PubMed)
DOI: DOI:10.4049/jimmunol.1700806   (Journal Full-text)

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.

Disease Annotations    
Entamoebiasis  (IMP,ISO)

Objects Annotated

Genes (Rattus norvegicus)
Ifng  (interferon gamma)

Genes (Mus musculus)
Ifng  (interferon gamma)

Genes (Homo sapiens)
IFNG  (interferon gamma)

Additional Information