2001: Coinfection with Borrelia burgdorferi and the agent of human granulocytic ehrlichiosis

1: Infect Immun. 2001 May;69(5):3359-71. Related Articles, Links


Coinfection with Borrelia burgdorferi and the agent of human
granulocytic ehrlichiosis alters murine immune responses, pathogen
burden, and severity of Lyme arthritis.

Thomas V, Anguita J, Barthold SW, Fikrig E.

Section of Rheumatology, Department of Internal Medicine, Yale
University School of Medicine, New Haven, Connecticut 06520, USA.

Lyme disease and human granulocytic ehrlichiosis (HGE) are tick-borne
illnesses caused by Borrelia burgdorferi and the agent of HGE,
respectively. We investigated the influence of dual infection with B.
burgdorferi and the HGE agent on the course of murine Lyme arthritis
and granulocytic ehrlichiosis. Coinfection resulted in increased levels
of both pathogens and more severe Lyme arthritis compared with those in
mice infected with B. burgdorferi alone. The increase in bacterial
burden during dual infection was associated with enhanced acquisition
of both organisms by larval ticks that were allowed to engorge upon
infected mice. Coinfection also resulted in diminished interleukin-12
(IL-12), gamma interferon (IFN-gamma), and tumor necrosis factor alpha
levels and elevated IL-6 levels in murine sera. During dual infection,
IFN-gamma receptor expression on macrophages was also reduced, implying
a decrease in phagocyte activation. These results suggest that
coinfection of mice with B. burgdorferi and the HGE agent modulates
host immune responses, resulting in increased bacterial burden, Lyme
arthritis, and pathogen transmission to the vector.

PMID: 11292759 [PubMed - indexed for MEDLINE]

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