The selectin family of adhesion molecules mediates the initial attachment o
f leukocytes to venular endothelial cells at sites of tissue injury and inf
lammation. To assess the role of selectin family in Staphylococcus aureus-t
riggered septic arthritis, we used several approaches. First, treatment wit
h fucoidin, a carbohydrate molecule capable of binding to and blocking sele
ctin functions, was used, in addition, we used P-selectin gene-targeted mic
e as well as mice pretreated with monoclonal antibody blocking L-selectin f
unction. The P-selectin-deficient and fucoidin-treated animals initially ex
hibited a less severe septic arthritis both clinically and histopathologica
lly. In the later stages of the disease no significant differences with res
pect to arthritis were evident. Pretreatment with L-selectin blocking antib
ody did not influence the severity of arthritis. High numbers of staphyloco
cci were recovered from the kidneys of selectin-deficient mice, indicating
a less efficient clearance of bacteria. Our results demonstrate a dual role
for selectins in S. aureus-induced arthritis: on the one hand, blockade of
these selectins leads to less severe arthritic lesions in the initial stag
e of the disease; on the other, delayed recruitment of phagocytes decreases
the clearance of bacteria.