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Am J Physiol Lung Cell Mol Physiol (August 9, 2002). doi:10.1152/ajplung.00016.2002
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Articles in PresS, published online ahead of print August 9, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00016.2002
Submitted on January 14, 2002
Accepted on August 1, 2002

Involvement of CD40-CD40L Signaling in Post-Ischemic Lung Injury

Timothy M. Moore1, W. Bradley Shirah1, Pavel L. Khimenko1, Peyton Paisley1, Robert N. Lausch2, and Aubrey E. Taylor1*

1 Department of Physiology, University of South Alabama College of Medicine, Mobile, AL, USA
2 Microbiology and Immunology, University of South Alabama College of Medicine, Mobile, AL, USA

* To whom correspondence should be addressed. E-mail: ataylor{at}jaguar1.usouthal.edu.

Our studies show that 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 pro-inflammatory events, results in significantly lower post-ischemic Kf,c values. Antagonism of CD40-CD40L signaling also results in attenuation of I/R-elicited macrophage inflammatory protein-2 (MIP-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 pre-treating 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 post-ischemic 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.




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