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Citations to this article

Clostridium difficile toxin A-induced microvascular dysfunction. Role of histamine.
I Kurose, … , R Wolf, D N Granger
I Kurose, … , R Wolf, D N Granger
Published November 1, 1994
Citation Information: J Clin Invest. 1994;94(5):1919-1926. https://doi.org/10.1172/JCI117542.
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Research Article

Clostridium difficile toxin A-induced microvascular dysfunction. Role of histamine.

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Abstract

Clostridium difficile toxin A (Tx-A) mediates secretion and inflammation in experimental enterocolitis. Intravital video microscopy was used to define the mechanisms that underlie the inflammatory reactions elicited by direct exposure of the microvasculature to Tx-A. Leukocyte adherence and emigration, leukocyte-platelet aggregation, and extravasation of FITC-albumin were monitored in rat mesenteric venules exposed to Tx-A. Significant increases in leukocyte adherence and emigration (LAE) and albumin leakage were noted within 15-30 min of Tx-A exposure. These responses were accompanied by mast cell degranulation and the formation of platelet-leukocyte aggregates. The Tx-A-induced increases in LAE and albumin leakage were significantly attenuated by pretreatment with either monoclonal antibodies (mAbs) directed against the leukocyte adhesion glycoproteins, CD11/CD18, intercellular adhesion molecule-1, and P-selectin (but not E-selectin) or with sialyl Lewis x, a counter-receptor for P-selectin. The mast cell stabilizer, lodoxamide, an H1- (but not an H2-) receptor antagonist, and diamine oxidase (histaminase) were also effective in reducing the LAE and albumin leakage elicited by Tx-A. The platelet-leukocyte aggregation response was blunted by an mAb against P-selectin, sialyl Lewis x, and the H1-receptor antagonist. These observations indicate that Tx-A induces a leukocyte-dependent leakage of albumin from postcapillary venules. Mast cell-derived histamine appears to mediate at least part of the leukocyte-endothelial cell adhesion and platelet-leukocyte aggregation by engaging H1-receptors on endothelial cells and platelets to increase the expression of P-selectin. The adhesion glycoproteins CD11/CD18 and intercellular adhesion molecule-1 also contribute to the inflammatory responses elicited by toxin A.

Authors

I Kurose, C Pothoulakis, J T LaMont, D C Anderson, J C Paulson, M Miyasaka, R Wolf, D N Granger

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Total citations by year

Year: 2024 2021 2019 2018 2017 2016 2015 2014 2012 2011 2010 2009 2008 2007 2006 2004 2003 2001 2000 1999 1998 1997 1996 1995 1991 Total
Citations: 2 1 1 1 1 1 1 3 3 1 1 2 2 2 3 4 3 3 1 5 6 3 5 1 1 57
Citation information
This citation data is accumulated from CrossRef, which receives citation information from participating publishers, including this journal. Not all publishers participate in CrossRef, so this information is not comprehensive. Additionally, data may not reflect the most current citations to this article, and the data may differ from citation information available from other sources (for example, Google Scholar, Web of Science, and Scopus).

Citations to this article in year 2016 (1)

Title and authors Publication Year
Thrombocytopenia in hospitalized patients with severe clostridium difficile infection
EM Fountain, MC Moses, LP Park, CW Woods, GM Arepally
Journal of Thrombosis and Thrombolysis 2016

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