Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice

Background Helicobacter cinaedi, an enterohepatic helicobacter species (EHS), is an important human pathogen and is associated with a wide range of diseases, especially in immunocompromised patients. It has been convincingly demonstrated that innate immune response to certain pathogenic enteric b...

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Main Authors: Shen, Zeli, Feng, Yan, Rickman, Barry H, Fox, James G
Other Authors: Massachusetts Institute of Technology. Division of Comparative Medicine
Format: Article
Language:en_US
Published: Wiley Blackwell 2017
Online Access:http://hdl.handle.net/1721.1/109464
https://orcid.org/0000-0001-9307-6116
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author Shen, Zeli
Feng, Yan
Rickman, Barry H
Fox, James G
author2 Massachusetts Institute of Technology. Division of Comparative Medicine
author_facet Massachusetts Institute of Technology. Division of Comparative Medicine
Shen, Zeli
Feng, Yan
Rickman, Barry H
Fox, James G
author_sort Shen, Zeli
collection MIT
description Background Helicobacter cinaedi, an enterohepatic helicobacter species (EHS), is an important human pathogen and is associated with a wide range of diseases, especially in immunocompromised patients. It has been convincingly demonstrated that innate immune response to certain pathogenic enteric bacteria is sufficient to initiate colitis and colon carcinogenesis in recombinase-activating gene (Rag)-2-deficient mice model. To better understand the mechanisms of human IBD and its association with development of colon cancer, we investigated whether H. cinaedi could induce pathological changes noted with murine enterohepatic helicobacter infections in the Rag2[superscript −/−] mouse model. Materials and Methods Sixty 129SvEv Rag2[superscript −/−] mice mouse were experimentally or sham infected orally with H. cinaedi strain CCUG 18818. Gastrointestinal pathology and immune responses in infected and control mice were analyzed at 3, 6 and 9 months postinfection (MPI). H. cinaedi colonized the cecum, colon, and stomach in infected mice. Results H. cinaedi induced typhlocolitis in Rag2[superscript −/−] mice by 3 MPI and intestinal lesions became more severe by 9 MPI. H. cinaedi was also associated with the elevation of proinflammatory cytokines, interferon-γ, tumor-necrosis factor-α, IL-1β, IL-10; iNOS mRNA levels were also upregulated in the cecum of infected mice. However, changes in IL-4, IL-6, Cox-2, and c-myc mRNA expressions were not detected. Conclusions Our results indicated that the Rag2[superscript −/−] mouse model will be useful to continue investigating the pathogenicity of H. cinaedi, and to study the association of host immune responses in IBD caused by EHS.
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spelling mit-1721.1/1094642022-09-29T09:53:31Z Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice Shen, Zeli Feng, Yan Rickman, Barry H Fox, James G Massachusetts Institute of Technology. Division of Comparative Medicine Shen, Zeli Feng, Yan Rickman, Barry H Fox, James G Background Helicobacter cinaedi, an enterohepatic helicobacter species (EHS), is an important human pathogen and is associated with a wide range of diseases, especially in immunocompromised patients. It has been convincingly demonstrated that innate immune response to certain pathogenic enteric bacteria is sufficient to initiate colitis and colon carcinogenesis in recombinase-activating gene (Rag)-2-deficient mice model. To better understand the mechanisms of human IBD and its association with development of colon cancer, we investigated whether H. cinaedi could induce pathological changes noted with murine enterohepatic helicobacter infections in the Rag2[superscript −/−] mouse model. Materials and Methods Sixty 129SvEv Rag2[superscript −/−] mice mouse were experimentally or sham infected orally with H. cinaedi strain CCUG 18818. Gastrointestinal pathology and immune responses in infected and control mice were analyzed at 3, 6 and 9 months postinfection (MPI). H. cinaedi colonized the cecum, colon, and stomach in infected mice. Results H. cinaedi induced typhlocolitis in Rag2[superscript −/−] mice by 3 MPI and intestinal lesions became more severe by 9 MPI. H. cinaedi was also associated with the elevation of proinflammatory cytokines, interferon-γ, tumor-necrosis factor-α, IL-1β, IL-10; iNOS mRNA levels were also upregulated in the cecum of infected mice. However, changes in IL-4, IL-6, Cox-2, and c-myc mRNA expressions were not detected. Conclusions Our results indicated that the Rag2[superscript −/−] mouse model will be useful to continue investigating the pathogenicity of H. cinaedi, and to study the association of host immune responses in IBD caused by EHS. United States. National Institutes of Health (R01-0D011141) United States. National Institutes of Health (R01-CA067529) United States. National Institutes of Health (P30-ES002109) United States. National Institutes of Health (P01-CA026731) 2017-05-31T15:41:26Z 2017-05-31T15:41:26Z 2015-03 Article http://purl.org/eprint/type/JournalArticle 1083-4389 1523-5378 http://hdl.handle.net/1721.1/109464 Shen, Zeli; Feng, Yan; Rickman, Barry and Fox, James G. “ Helicobacter Cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice .” Helicobacter 20, no. 2 (November 2014): 146–155 © 2014 John Wiley & Sons Ltd https://orcid.org/0000-0001-9307-6116 en_US http://dx.doi.org/10.1111/hel.12179 Helicobacter Creative Commons Attribution-Noncommercial-Share Alike http://creativecommons.org/licenses/by-nc-sa/4.0/ application/pdf Wiley Blackwell PMC
spellingShingle Shen, Zeli
Feng, Yan
Rickman, Barry H
Fox, James G
Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title_full Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title_fullStr Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title_full_unstemmed Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title_short Helicobacter cinaedi Induced Typhlocolitis in Rag-2-Deficient Mice
title_sort helicobacter cinaedi induced typhlocolitis in rag 2 deficient mice
url http://hdl.handle.net/1721.1/109464
https://orcid.org/0000-0001-9307-6116
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