Interleukin-10 inhibits proinflammatory activation of endothelium in response to Borrelia burgdorferi or lipopolysaccharide but not interleukin-1β or tumor necrosis factor α

• Published in: Journal of leukocyte biology Vol. 72; no. 3; pp. 503 - 511
• Main Authors: Lisinski, Tracy J., Furie, Martha B.
• Format: Journal Article
• Language: English
• Published: Society for Leukocyte Biology 01.09.2002
• Subjects: adhesion molecules; chemokines; leukocytes
• ISSN: 0741-5400; 1938-3673
• DOI: 10.1189/jlb.72.3.503

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‐lβ or tumor necrosis factor α. 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.