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Infection and Immunity, February 1999, p. 726-732, Vol. 67, No. 2
National Public Health
Institute1 and
MediCity Research
Laboratory, University of Turku,2 Turku,
Finland
Received 10 September 1997/Returned for modification 24 November
1997/Accepted 21 October 1998
Reactive arthritis is usually a self-limiting polyarthritis which
develops after certain gastrointestinal or urogenital infections. Microbial antigens found in the inflamed joints are thought to play a
key role in the development of this disease. It is not known how
antigens of the pathogenic organisms migrate from the mucosal tissues
into the joints. The data presented here show that mononuclear
phagocytes which mediate the dissemination of several intracellular
pathogens acquire an enhanced capacity to bind to nonstimulated
vascular endothelial cells after phagocytosis of
Yersinia enterocolitica O:3, one of the causative organisms of reactive arthritis. The increased binding to previously
nonstimulated endothelial cells was mediated by P-selectin, whose
translocation to the endothelial cell surface was induced by monocytes
with intracellular Yersinia bacteria. These results suggest
that mononuclear phagocytes may be responsible for the dissemination of
bacterial antigens and the initiation of the joint
inflammation in reactive arthritis.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Monocytes That Have Ingested Yersinia enterocolitica
Serotype O:3 Acquire Enhanced Capacity To Bind to Nonstimulated
Vascular Endothelial Cells via P-Selectin
*
Corresponding author. Mailing address: MediCity
Research Laboratory, University of Turku, Tykistökatu 6, FIN-20520 Turku, Finland. Phone: 358-2-3337007. Fax:
358-2-3337000. E-mail: sirpa.jalkanen{at}utu.fi.
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