NDLI: TRPV1 deletion enhances local inflammation and accelerates the onset of systemic inflammatory response syndrome.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Alam, Saydul Riffo-Vasquez, Yanira Purcell, Robert Collins, Helen Liang, Lihuan Rivett, Damian W. Fernandes, Elizabeth S. Smillie, Sarah-Jane Kaiser, Frank Keeble, Julie E. Howat, Sarah Brain, Susan D. Thompson, Stephen J. Bruce, Kenneth D.
Description	Country affiliation: United kingdom Author Affiliation: Fernandes ES ( British Heart Foundation Centre for Cardiovascular Research, King's College London, London SE1 9NH, United Kingdom.)
Abstract	The transient receptor potential vanilloid 1 (TRPV1) is primarily localized to sensory nerve fibers and is associated with the stimulation of pain and inflammation. TRPV1 knockout (TRPV1KO) mice show enhanced LPS-induced sepsis compared with wild type (WT). This implies that TRPV1 may have a key modulatory role in increasing the beneficial and reducing the harmful components in sepsis. We investigated immune and inflammatory mechanisms in a cecal ligation and puncture (CLP) model of sepsis over 24 h. CLP TRPV1KO mice exhibited significant hypothermia, hypotension, and organ dysfunction compared with CLP WT mice. Analysis of the inflammatory responses at the site of initial infection (peritoneal cavity) revealed that CLP TRPV1KO mice exhibited: 1) decreased mononuclear cell integrity associated with apoptosis, 2) decreased macrophage tachykinin NK(1)-dependent phagocytosis, 3) substantially decreased levels of nitrite (indicative of NO) and reactive oxygen species, 4) increased cytokine levels, and 5) decreased bacteria clearance when compared with CLP WT mice. Therefore, TRPV1 deletion is associated with impaired macrophage-associated defense mechanisms. Thus, TRPV1 acts to protect against the damaging impact of sepsis and may influence the transition from local to a systemic inflammatory state.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	11
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Systemic Inflammatory Response Syndrome Immunology Pathology Trpv Cation Channels Deficiency Genetics Up-regulation Animals Mice Mice, 129 Strain Mice, Inbred C57bl Mice, Knockout Nitric Oxide Antagonists & Inhibitors Peritoneum Surgery Reactive Oxygen Species Biosynthesis Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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