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(Journal of Leukocyte Biology. 2002;72:503-511.)
© 2002 by Society for Leukocyte Biology

Interleukin-10 inhibits proinflammatory activation of endothelium in response to Borrelia burgdorferi or lipopolysaccharide but not interleukin-1ß or tumor necrosis factor {alpha}

Tracy J. Lisinski and Martha B. Furie

Center for Infectious Diseases and Department of Pathology, State University of New York at Stony Brook

Correspondence: Tracy J. Lisinski, Center for Infectious Diseases/CMM, SUNY at Stony Brook, Stony Brook, NY 11794-5120. E-mail: tlisinsk{at}notes.cc.sunysb.edu

Interleukin (IL)-10 is generally regarded as an anti-inflammatory cytokine, since it acts on a variety of cell types to suppress production of proinflammatory mediators. In inflammation, endothelial cells (EC) play a crucial role in recruiting leukocytes to sites of injury or infection. In this study, the actions of IL-10 on human umbilical vein EC were investigated. IL-10 reduced migration of monocytes and T lymphocytes across endothelium stimulated by lipopolysaccharide and decreased endothelial production of chemokines in response to lipopolysaccharide and Borrelia burgdorferi, the agent of Lyme disease. However, IL-10 did not affect these responses when EC were activated by the host proinflammatory cytokines IL-lß or tumor necrosis factor {alpha}. Moreover, IL-10 did not prevent up-regulation of the adhesion molecules E-selectin and intercellular adhesion molecule-1 by EC exposed to any of these activating agents. IL-10 therefore inhibits proinflammatory activation of EC in a manner that is selective with respect to stimulus and effector response.

Key Words: chemokines • leukocytes • adhesion molecules




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