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Am J Physiol Heart Circ Physiol (September 19, 2005). doi:10.1152/ajpheart.00701.2005
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Submitted on June 28, 2005
Accepted on September 9, 2005

Cellular and Molecular Mechanisms Underlying LPS-Associated Myocyte Impairment

Samantha A Tavener1 and Paul Kubes1*

1 Physiology & Biophysics, University of Calgary, Calgary, Alberta, Canada

* To whom correspondence should be addressed. E-mail: pkubes{at}ucalgary.ca.

Recently we reported that Toll-like Receptor 4 (TLR4) positive immune cells of unknown identity were responsible for the LPS-induced depression of cardiac myocyte shortening. The aim of this study is to identify the TLR4-positive cell type that is responsible for the LPS-induced cardiac dysfunction. Neither neutrophil depletion alone nor mast cell deficiency had any impact on the impairment of myocyte shortening during LPS treatment. In contrast, LPS-treated macrophage deficient mice demonstrated a partial reduction in shortening compared to saline-treated macrophage deficient mice. Since the removal of macrophages could only partially restore myocyte shortening, we also investigated the effects of removing both neutrophils and macrophages on myocyte shortening. Interestingly, endotoxemic, neutrophil depleted, macrophage deficient mice had completely restored myocyte shortening. Since both macrophages and neutrophils can produce nitric oxide (NO) and TNF-{alpha} we examined LPS-treated inducible nitric oxide synthase knock out (iNOSKO) mice and TNF receptor deficient mice. Eliminating both TNF receptors (TNFR1 and TNFR2) was required to restore myocyte shortening during LPS treatment whereas iNOS deficiency had no effect. These data suggest that macrophages and to a lesser degree neutrophils cause cardiac impairment presumably via TNF-{alpha}.




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