Analyzing the innate immunity of NIH hairless mice and the impact of gut microbial polymorphisms on Listeria monocytogenes infection
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Zhong-Hao Ji1, Wen-Zhi Ren1, Wei Gao1, Yang Hao1, Wei Gao1, Jian Chen1, Fu-Shi Quan1, Jin-Ping Hu1 and Bao Yuan1
1Department of Laboratory Animals, College of Animal Sciences, Jilin University, Changchun 130062, Jilin, China
Bao Yuan, email: [email protected]
Keywords: NIH hairless mice; Listeria monocytogenes; gut microbiota; 16S rRNA; innate immunity
Received: August 23, 2017 Accepted: October 03, 2017 Published: October 25, 2017
Spontaneous mutant hairless (HL) mice are often used to study hair growth and hair follicle development, and they often exhibit immune dysfunctions. Listeria monocytogenes, an important food-borne bacterium, has been used in animal models to study immune responses to infection. Herein, we analyzed the innate immunity of HL mice and the impact of gut microbial polymorphisms on L. monocytogenes infection. Compared to NIH mice, NIH HL mice were more susceptible to L. monocytogenes, as weight losses, mortality, bacterial load, and histopathological lesions were more severe; the decrease in monocytes may be an important underlying reason. The degree of spleen damage was reduced after co-housing, indicating that the host guides the gut microbiota to alleviate infection. High-throughput pyrosequencing of 16S rRNA demonstrated that gut microbiota composition differed between NIH HL and NIH mice. Infection with L. monocytogenes induced an increase in the number of bacteria belonging to the Rikenellaceae family and Gammaproteobacteria class, and decreased bacteria belonging to the Clostridiales class and Lachnospiraceae family. A substantial reduction in Clostridiales bacteria in infected HL mice may cause a serious infection. The Mycoplasma genus was present only in NIH HL mice and was, thus, considered a biomarker. The results of this study improve our understanding of the use of NIH HL mice as a good animal model of innate immune dysfunction.
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