Current status of pathogenetic mechanisms in staphylococcal arthritis.
Interactions between staphylococci and the joint tissues of the host lead typically to rapidly progressing and highly destructive processes. Staphylococci possess a vast arsenal of components and products that contribute to the pathogenesis of joint infection. Occasionally these compounds have overlapping activities and act either in concert or alone. Host responsiveness to staphylococcal infection displays an even more complex pattern. Most of the cells and molecules that participate in the innate immune system protect the host against bacteria. However, the staphylococci have developed systems that counteract endogenous protective mechanisms. Interestingly, certain cells and molecules of the acquired immune system potentiate the severity of infection by triggering exaggerated responses to the staphylococcal danger signals. This review deals with the intricate host-bacterium interactions that occur during experimental septic arthritis, and outlines potential preventive and treatment modalities.
Tarkowski
Andrej
A
Department of Rheumatology and Inflammation Research, University of Göteborg, Guldhedsgatan 10, 413 46 Göteborg, Sweden. andrej.tarkowski@microbio.gu.se
Bokarewa
Maria
M
Collins
L Vincent
LV
Gjertsson
Inger
I
Hultgren
Olof H
OH
Jin
Tao
T
Jonsson
Ing-Marie
IM
Josefsson
Elisabet
E
Sakiniene
Egidija
E
Verdrengh
Margareta
M
D000818:Animals; D001170:Arthritis, Infectious / Q000276:immunology / Q000382:microbiology* / Q000628:therapy; D018925:Chemokines / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D007110:Immunity, Active; D007596:Joints / Q000382:microbiology; D051379:Mice; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology* / Q000628:therapy; D013210:Staphylococcus / Q000145:classification / Q000378:metabolism / Q000472:pathogenicity*; D016896:Treatment Outcome; D037521:Virulence Factors / Q000378:metabolism
D018925:Chemokines; D016207:Cytokines; D037521:Virulence Factors