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Incubation of human umbilical vein endothelial cells (HUVEC) cultured on amniotic tissue with either interleukin-1 (IL-1) or<jats:italic>Borrelia burgdorferi<\/jats:italic>, the spirochetal agent of Lyme disease, increased the rate at which human monocytes migrated across the endothelial monolayers. Very late antigen 4 (VLA-4) and CD11\/CD18 integrins mediated migration of monocytes across HUVEC exposed to either<jats:italic>B. burgdorferi<\/jats:italic>or IL-1 in similar manners. Neutralizing antibodies to the chemokine monocyte chemoattractant protein 1 (MCP-1) inhibited the migration of monocytes across unstimulated, IL-1-treated, or<jats:italic>B. burgdorferi<\/jats:italic>-stimulated HUVEC by 91% \u00b1 3%, 65% \u00b1 2%, or 25% \u00b1 22%, respectively. Stimulation of HUVEC with<jats:italic>B. burgdorferi<\/jats:italic>also promoted a 6-fold \u00b1 2-fold increase in the migration of human CD4<jats:sup>+<\/jats:sup>T lymphocytes. Although MCP-1 played only a limited role in the migration of monocytes across<jats:italic>B. burgdorferi<\/jats:italic>-treated HUVEC, migration of CD4<jats:sup>+<\/jats:sup>T lymphocytes across HUVEC exposed to spirochetes was highly dependent on this chemokine. The anti-inflammatory cytokine IL-10 reduced both migration of monocytes and endothelial production of MCP-1 in response to<jats:italic>B. burgdorferi<\/jats:italic>by approximately 50%, yet IL-10 inhibited neither migration nor secretion of MCP-1 when HUVEC were stimulated with IL-1. Our results suggest that activation of endothelium by<jats:italic>B. burgdorferi<\/jats:italic>may contribute to formation of the chronic inflammatory infiltrates associated with Lyme disease. The transendothelial migration of monocytes that is induced by<jats:italic>B. burgdorferi<\/jats:italic>is significantly less dependent on MCP-1 than is migration induced by IL-1. Selective inhibition by IL-10 further indicates that<jats:italic>B. burgdorferi<\/jats:italic>and IL-1 employ distinct mechanisms to activate endothelial cells.<\/jats:p>","DOI":"10.1128\/iai.66.10.4875-4883.1998","type":"journal-article","created":{"date-parts":[[2019,12,31]],"date-time":"2019-12-31T15:20:47Z","timestamp":1577805647000},"page":"4875-4883","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":17,"title":["<i>Borrelia burgdorferi<\/i>and Interleukin-1 Promote the Transendothelial Migration of Monocytes In Vitro by Different Mechanisms"],"prefix":"10.1128","volume":"66","author":[{"given":"Margaret J.","family":"Burns","sequence":"first","affiliation":[{"name":"<!--label omitted: 1-->Department of Pathology, School of Medicine, State University of New York at Stony Brook, Stony Brook, New York 11794"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martha B.","family":"Furie","sequence":"additional","affiliation":[{"name":"<!--label omitted: 1-->Department of Pathology, School of Medicine, State University of New York at Stony Brook, Stony Brook, New York 11794"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"531","article-title":"Lyme disease\u2014United States, 1996","volume":"46","author":"Anonymous","year":"1997","unstructured":"Anonymous Lyme disease\u2014United States, 1996.Morbid. 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