Attenuation of H-Pylori-Induced Gastric Pathology in C57bl/6 Mice by Co-Infection with Enterohepatic Helicobacters Is Helicobacter Species-Dependent
Name
HpHm-Hh-V5.pdf
Size
277.29 KB
Format
Adobe PDF
Checksum (MD5)
4682f10ab598cc84629762b6a315994b
Author(s)
Ge, Zhongming
Feng, Yan
Muthupalani, Sureshkumar
Lemke, Laura B.
Whary, Mark T.
Fox, James G.
Date Issued
July 2010
Journal
Helicobacter
Publisher
Wiley-Blackwell Publishers
Citation
Ge, Zhongming, Yang Feng, Sureshkumar Muthupalani, Laura B. Lemke, Mark T. Whary, and James G. Fox. "Attenuation of H. pylori-induced gastric pathology in C57BL/6 mice by co-infection with enterohepatic helicobacters is Helicobacter species-dependent." In XXIII International Workshop on Helicobacter and Related Bacteria in Chronic Digestive Inflammation and Gastric Cancer [Abstracts], Rotterdam, September 16–18, 2010, Helicobacter 15.4 (2010) p. 317.
Version
Author's final manuscript
Abstract
To investigate how concurrent infection with an enterohepatic
helicobacter species (EHS) affects H. pylori (Hp)-induced gastric
pathology, C57BL/6 mice were inoculated with H. hepaticus
(Hh), or H. muridarum (Hm), followed by infection with Hp.
Compared to Hp-infected mice, HmHp-infected mice at 6 and
11 months postinoculation (mpi) had markedly attenuated
histopathologic activity index (HAI) scores (P < 0.0001). By
contrast, HhHp-infected mice had more severe HAI scores
(P = 0.01) at 6 mpi and had similar HAI scores (P = 0.8) at
11 mpi when compared to Hp-infected mice. Hm-mediated
attenuated pathology was associated with significant downregulation
of proinflammatory Th1 (IL1, IFN[[Unsupported
Character - ]] and TNF) and Th17 (IL-17A) cytokine
mRNA levels in stomachs when compared to the Hp-infected
mice. Although co-infection with Hh suppressed Hp-induced
elevation of gastric Th1 cytokines, Th17 cytokine mRNA levels
were increased. Colonization levels of gastric Hp were increased
in both HhHp- and HmHp-infected mice compared to mono-
Hp-infected mice. The Hp levels correlated with the mRNA levels
of the gastric proinflammatory Th1 cytokines. Furthermore, the
mRNA levels of IL17A were positively correlated with the
severity of helicobacter-induced gastric pathology (HhHp>Hp>
HmHp). Our data suggest: (1) host Th1 responses plays a major
role in limiting Hp colonization; (2) EHS-mediated attenuation
of the Hp-induced gastric pathology depends on the ability of the
individual EHS to suppress both Th1 and IL17 proinflammatory
pathways.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Massachusetts Institute of Technology. Division of Comparative Medicine
Terms of Use
Creative Commons Attribution-Noncommercial-Share Alike 3.0
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1111/j.1523-5378.2010.00771.x/pdf
