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Infiltration of macrophages through the atrial endocardium of inflammation-induced rats: contribution of fractalkine.

Authors: Date, T  Yamashita, T  Sekiguchi, A  Iwasaki, YK  Aizawa, T  Yamane, T  Aramaki, Y  Komukai, K  Taniguchi, I  Yoshimura, M 
Citation: Date T, etal., Circ J. 2009 May;73(5):932-7. Epub 2009 Mar 12.
Pubmed: (View Article at PubMed) PMID:19282612

BACKGROUND: Inflammatory processes in the atria during systemic inflammation remain unclear, so this study tested the hypothesis that macrophages infiltrate the atrial myocardium mainly through the atrial endocardium with the contribution of fractalkine. METHODS AND RESULTS: Sprague-Dawley rats were injected with lipopolysaccharide (LPS) to simulate inflammation in the atria. Inflammation was immunohistologically assessed by the presence of macrophages. Macrophage infiltration was diffuse throughout the atrial myocardium after LPS injection. At an earlier phase after LPS injection, the number of macrophages dramatically increased, mainly in the atrial endocardium, and the expression of fractalkine protein was markedly increased by treatment with LPS in the atrial endocardium. The LPS-induced increase in atrial macrophage infiltration was significantly suppressed by neutralizing the fractalkine protein (P<0.01). CONCLUSIONS: In an experimental model of atrial inflammation, macrophages infiltrated the myocardium mainly through the atrial endocardium with the contribution of fractalkine. Inhibition of macrophage infiltration by suppressing chemokine expression could be a novel therapeutic approach to controling acute inflammation in the atria.

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RGD Object Information
RGD ID: 4891965
Created: 2011-01-25
Species: All species
Last Modified: 2011-01-25
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.