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Am J Physiol Lung Cell Mol Physiol 283: L1255-L1262, 2002. First published August 9, 2002; doi:10.1152/ajplung.00016.2002
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Vol. 283, Issue 6, L1255-L1262, December 2002

Involvement of CD40-CD40L signaling in postischemic lung injury

Timothy M. Moore, W. Bradley Shirah, Pavel L. Khimenko, Peyton Paisley, Robert N. Lausch, and Aubrey E. Taylor

Department of Physiology, University of Alabama College of Medicine, Mobile, Alabama 36688-0002

Our studies show that ischemia-reperfusion (I/R) in the isolated rat lung causes retention of lymphocytes, which is associated with increased microvascular permeability, as determined by quantitative measurement of the microvascular filtration coefficient (Kf,c). Immunoneutralization of either CD40 or CD40L, cell surface proteins important in lymphocyte-endothelial cell proinflammatory events, results in significantly lower postischemic Kf,c values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 production. Rat lymphocytes activated ex vivo with phorbol 12-myristate, 13-acetate increased Kf,c in isolated lungs independently of I/R, and this increase was prevented by pretreating lungs with anti-CD40. In addition to lymphocyte involvement via CD40-CD40L interactions, our studies also show that I/R injury is potentiated by antagonism of IL-10 produced locally within the postischemic lung, whereas exogenous, rat recombinant IL-10 provided protection against I/R-induced microvascular damage. Thus acute lymphocyte involvement in lung I/R injury involves CD40-CD40L signaling mechanisms, and these events may be influenced by local IL-10 generation.

inflammation; filtration coefficient; lymphocytes; macrophage inflammatory protein-2


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