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The effect of Helicobacter typhlonius infection on colonic ion transport in the IL10 knockout mice
Author(s) -
Lindstrom Anna,
Fan Shujun,
Schultz Michael,
Butt Grant
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1109.1
Subject(s) - inflammation , interleukin 10 , knockout mouse , immunology , colitis , medicine , distal colon , chemistry , cytokine , receptor
Helicobacter infection causes severe colitis in immunocompromised mice, but little is know of its effects on the properties of the colonic epithelium. We compared the effects of H. typhlonius infection on the functional properties of the proximal (PC) and distal colon (DC) of wildtype (WT) and IL10 knockout (IL10 −/− ) mice. WT mice showed no clinical effects of infection, colonic inflammation or changes in functional properties of the colon. Other than a slight increase in water content of the stool, IL10 −/− mice also showed no clinical effects of infection. Despite this the PC was severely inflamed, with a milder inflammation in the DC. There was no increase in TNFα or INFγ associated with the inflammation, but IL12p40 levels were increased. Unexpectedly, the conductance (G T ) of the PC was decreased, as was the permeability. No change in G T of the DC occurred. Associated with infection was a reduction in the spontaneous short circuit current (I sc ) in the PC but not the DC. Also, in the PC of infected animals the forskolin‐stimulated I sc was only ≈5% of that of non‐infected controls, whereas the response of the DC was ≈50% of that of controls. In contrast, in infected animals the carbachol‐stimulated I sc was essentially eliminated in both the PC and DC. As seen in other inflammatory models colonic inflammation associated with H. typhlonius infection of IL10 −/− mice markedly alters the transport properties of the colon, however this does not result in diarrhea. This may be a consequence of the absence of a change in colonic permeability or distal sparing due to the limited inflammation in the distal colon. Supported by the University of Otago.