2006: Host Inflammatory Response against Infection with Lyme

1: Infect Immun. 2006 Feb;74(2):1156-60. Links


Fas Ligand Deficiency Impairs Host Inflammatory Response against
Infection with the Spirochete Borrelia burgdorferi.

Shi C, Wolfe J, Russell JQ, Fortner K, Hardin N, Anguita J, Budd RC.

Immunobiology Program, The University of Vermont College of Medicine,
Given Medical Building, Burlington, VT 05405-0068. ralph.budd@xxxxxxxx

Lyme disease represents a complex response to Borrelia burgdorferi that
involves both bacterial factors as well as host responses. This results
in an inflammatory reaction at several sites, including the synovial
lining of joints. Synovial tissues of inflamed joints contain cells
expressing high levels of Fas and Fas ligand (FasL). Although Fas
stimulation is typically associated with cell death, it can also
transmit stimulatory signals to certain cell types. Among these are
dendritic cells and macrophages, which are abundant in inflamed
synovium. To better assess the role of FasL in the pathogenesis of Lyme
arthritis, we evaluated the response to B. burgdorferi infection in
C3H/HeJgld mice that bear a nonfunctional mutation in FasL. Compared to
wild-type C3H(+/+) mice, C3Hgld mice had a similar bacterial burden and
antibody response 2 weeks and 4 weeks following infection, but they
manifested a significantly reduced Borrelia-specific cytokine response.
In addition, C3Hgld mice developed a greatly reduced incidence and
severity of arthritis. The findings document a contribution of FasL to
the host inflammatory response to B. burgdorferi.

PMID: 16428764 [PubMed - in process]

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