Vanilloid receptor (TRPV1)-deficient mice show increased susceptibility to dinitrobenzene sulfonic acid induced colitis.
J Mol Med. 2005-12-31; 84(2): 142-146
DOI: 10.1007/s00109-005-0016-2
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1. J Mol Med (Berl). 2006 Feb;84(2):142-6. Epub 2005 Dec 31.
Vanilloid receptor (TRPV1)-deficient mice show increased susceptibility to
dinitrobenzene sulfonic acid induced colitis.
Massa F(1), Sibaev A, Marsicano G, Blaudzun H, Storr M, Lutz B.
Author information:
(1)Department of Physiological Chemistry, Johannes Gutenberg-University Mainz,
Duesbergweg 6, 55099, Mainz, Germany.
In the human colon, vanilloid receptor TRPV1 is overexpressed both in afferent
nerve terminals and in epithelial cells during inflammation. In the past years,
pharmacological experiments using TRPV1 agonists and antagonists revealed that
TRPV1 receptors may play proinflammatory and protective roles in the
gastrointestinal tract. Here, we applied a genetic approach to define the role of
TRPV1 and analyzed the effects of dinitrobenzene sulfonic acid (DNBS)-induced
colitis in TRPV1-deficient (TRPV1-/-) mice. Intrarectal infusion of DNBS induced
increased inflammation in TRPV1-/- mice compared to wild-type littermates
(TRPV1+/+) as evaluated by macroscopic scoring and myeloperoxidase assays. This
finding indicates that TRPV1 receptors are required for the protection within
sensory pathways that regulate the response following the initiation of colonic
inflammation. Electrophysiological recordings from circular smooth-muscle cells,
performed 8 and 24 h after DNBS treatment, revealed strong spontaneous
oscillatory action potentials in TRPV1-/- but not in TRPV1+/+ colons, indicating
an early TRPV1-mediated control of inflammation-induced irritation of
smooth-muscle activities. These unexpected results suggest that TRPV1 receptors
mediate endogenous protection against experimentally induced colonic
inflammation.
DOI: 10.1007/s00109-005-0016-2
PMID: 16389550 [Indexed for MEDLINE]