| JWissmille 2004-10-20, 11:09 am |
| Protective niche for Borrelia burgdorferi to evade humoral immunity.
Am J Pathol 2004 Sep;165(3):977-85 (ISSN: 0002-9440)
Liang FT; Brown EL; Wang T; Iozzo RV; Fikrig E
Department of Internal Medicine, Section of Rheumatology, Yale University
School of Medicine, New Haven, Connecticut, USA.
The Lyme disease spirochete, Borrelia burgdorferi, is an extracellular microbe
that causes persistent infection despite the development of strong immune
responses against the bacterium. B. burgdorferi expresses several
ligand-binding lipoproteins, including the decorin-binding proteins (Dbps) A
and B, which may mediate attachment to decorin, a major component of the host
extracellular matrix during murine infection. We show that B. burgdorferi was
better protected in the joints and skin, two tissues with a higher decorin
expression, than in the urinary bladder and heart, two tissues with a lower
decorin expression, during chronic infection of wild-type mice. Targeted
disruption of decorin alone completely abolished the protective niche in
chronically infected decorin-deficient mice but did not affect the spirochete
burden during early infection. The nature of protection appeared to be specific
because the spirochetes with higher outer surface protein C expression were not
protected while the protective niche seemed to favor the spirochetes with a
higher dbpA expression during chronic infection. These data suggest that
spirochetal DbpA may interact with host decorin during infection and such
interactions could be a mechanism that B. burgdorferi uses to evade humoral
immunity and establish chronic infection.
Indexing Check Tags: Comparative Study; Support, U.S. Gov't, P.H.S.
Language: English
MEDLINE Indexing Date: 200409
Publication Type: Owner: NLM
Publication Type: Journal Article
Grant ID: AI32947; AI49200; AI55959; AR49405; CCU618387
PreMedline Identifier: 0015331421
Journal Code: AIM; IM
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