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1 School of pharmacy, University of Pittsburgh, Center for Phamacogenetics and Department of Pharmaceutical Sciences, Pittsburgh, PA, USA
2 Department of environmental and Occupational Health, Graduate School of Public health, University of Pittsburgh, Pittsburgh, PA, USA
3 University of South Alabama College of Medicine, Department of Pharmacology,Center for lung biology, Mobile, AL, USA
* To whom correspondence should be addressed. E-mail: sol4{at}pitt.edu.
Although the CpG DNA immune response mediated by Toll-like receptor 9 (TLR9) has been extensively studied in a number of immune cells, the response to CpG DNA in endothelial cells (EC) is not well understood. In this study, we show that both mouse and rat lung EC display constitutive expression of TLR9 mRNA. Exposure to CpG DNA induced a potent proinflammatory response as manifested by an increased expression of IL-8 and ICAM-1 in mouse pulmonary endothelial cells (MLEC). The proinflammatary response was sensitive to chloroquine consistent with a role of endosomal contribution. A role for p38 MAPK and NF-
B pathway was apparent as the response was sensitive to
inhibitors of p38 MAPK and NF-B but was not affected by inhibitors of ERK1/2. A synergistic effect of CpG DNA and LPS on the inflammatory response is consistent with multiple TLR interaction in EC. This study suggests a possible role for CpG DNAmediated EC immune response in the host defense system. It also has important implication in plasmid DNA-mediated pulmonary endothelium gene transfer.
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