Effect of Borrelia burgdorferi OspC at the Site of Inoculation in Mouse Skin.
Summary of "Effect of Borrelia burgdorferi OspC at the Site of Inoculation in Mouse Skin."
The Borrelia burgdorferi surface lipoprotein OspC is a critical virulence factor, but its precise role in the establishment of B. burgdorferi infection remains unclear. To determine whether OspC affects the host response at the site of inoculation of the bacterium, the recruitment of macrophages and neutrophils, and the production of cytokines, were examined at the site of infection by wild-type, ospC mutant, and complemented mutant B. burgdorferi. Of the 21 cytokines tested, MCP-1, KC, and VEGF were found at increased levels at the site of inoculation of B. burgdorferi, and the levels varied with production of OspC at one or more time points over the one-week course of infection. The kinetics of expression and the dependence on OspC production by B. burgdorferi varied among the cytokines. The production of KC and MCP-1, and the appearance of monocytic infiltrates, correlated with the presence of the bacteria, rather than with OspC, specifically. In contrast, VEGF production was not correlated simply to the presence of the bacteria, and is influenced by the presence of OspC. In in vitro assays, OspC and B. burgdorferi expressing OspC stimulated growth of endothelial cells more than did the controls. These data suggest the possibility of a novel role for OspC in the life of B. burgdorferi at the interface of its mammalian and tick hosts.
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts; Division of Infectious Diseases, and Center for Infectious Disease Research, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI
This article was published in the following journal.
Name: Infection and immunity
- PubMed Source: http://www.ncbi.nlm.nih.gov/pubmed/20696825
- DOI: http://dx.doi.org/10.1128/IAI.00464-10
Medical and Biotech [MESH] Definitions
Borrelia Burgdorferi Group
Gram-negative helical bacteria, in the genus BORRELIA, that are the etiologic agents of LYME DISEASE. The group comprises many specific species including Borrelia afzelii, Borellia garinii, and BORRELIA BURGDORFERI proper. These spirochetes are generally transmitted by several species of ixodid ticks.
A specific species of bacteria, part of the BORRELIA BURGDORFERI GROUP, whose common name is Lyme disease spirochete.
Nervous system infections caused by tick-borne spirochetes of the BORRELIA BURGDORFERI GROUP. The disease may affect elements of the central or peripheral nervous system in isolation or in combination. Common clinical manifestations include a lymphocytic meningitis, cranial neuropathy (most often a facial neuropathy), POLYRADICULOPATHY, and a mild loss of memory and other cognitive functions. Less often more extensive inflammation involving the central nervous system (encephalomyelitis) may occur. In the peripheral nervous system, B. burgdorferi infection is associated with mononeuritis multiplex and polyradiculoneuritis. (From J Neurol Sci 1998 Jan 8;153(2):182-91)
An infectious disease caused by a spirochete, BORRELIA BURGDORFERI, which is transmitted chiefly by Ixodes dammini (see IXODES) and pacificus ticks in the United States and Ixodes ricinis (see IXODES) in Europe. It is a disease with early and late cutaneous manifestations plus involvement of the nervous system, heart, eye, and joints in variable combinations. The disease was formerly known as Lyme arthritis and first discovered at Old Lyme, Connecticut.
The grafting of skin in humans or animals from one site to another to replace a lost portion of the body surface skin.
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