. Author manuscript; available in PMC: 2014 Mar 3.

Published in final edited form as: Mucosal Immunol. 2010 Oct 13;4(1):22–30. doi: 10.1038/mi.2010.61

Table 1.

H. hepaticus- and H. bilis-associated IBD in mice^a

Genetic status of mice	Type of defect	Pathology	Reference
CD45RB (high)-reconstituted ICR defined flora scids	Reconstitution with naïve CD4⁺ T cell	Typhlocolitis	10
TCRα, B mutants	Abnormal T cell receptors	Typhlocolitis	88
Scid ICR-defined flora^b	Lack T and B cell	Typhlocolitis	89, 90
C57BL/IL-10^−/−^c	Knockout	Typhlocolitis	14, 18, 19, 36
129SvEv/Rag2^−/−	Knockout	Typhlocolitis, colon cancer	28, 56
C57BLRag2^−/−	Knockout	Typhlocolitis	14
IL-7^−/−/RAG-2^−/−	Double Knockout	None	27
A/JCr	Normal	Typhlitis	3
Swiss Webster gnotobiotic	Normal	Enterocolitis	91
129SvEv/NF-κβ (p50^−/−p65^+/-)	Double Knockout	Typhlocolitis	92
mdrla^−/−^d	Lack P-glycoprotein	Typhlocolitis	93
SMAD3^−/−^d	Knockout	Typhlocolitis, colon cancer	94

In mice of the same genetic status which had H. hepaticus (or other Helicobacter spp.)-negative microflora, no intestinaldisease was noted.

Mice infected with H. bilis also produced IBD⁸⁹.

IBD also produced in C57Bl/IL-10^−/− mice experimentally infected with a novel urease-negative Helicobacter sp.⁹⁵; now namedH. typhlonius ⁹⁶; also IBD produced with H. trogontum ⁹⁷ and H. cinaedi ⁷⁴.

H. bilis produces IBD⁹³, ⁹⁴, and colon cancer⁹⁴.