Changes in the expression of various activation-dependent surface markers h
ave been reported for polymorphonuclear neutrophils (PMN) isolated from syn
ovial fluid of patients with inflammatory joint diseases. We extend these f
indings to the expression of CD66 molecules and several other surface marke
rs. Three members of the CD66 family, namely CD66a, CD66b, and CD66c, showe
d an up to fourfold up-regulation on synovial fluid PMN compared with perip
heral blood PMN (PBG) of the same patients; CD59 was increased twofold, the
expression of CD16 did not change, whereas CD62L was reduced by more than
50% on synovial fluid PMN, It is interesting that CD66a, CD66b, and CD66c s
howed a coordinated expression on PEG of patients and controls and a coordi
nated up-regulation on synovial neutrophils, In contrast, after in vitro st
imulation of peripheral blood PMN with phorbol myristate acetate, CD66c was
much less up-regulated compared with CD66a and CD66b, All samples of synov
ial fluid PMN exhibited an additional increase in the expression of CD66a,
CD66b, and CD66c when stimulated with phorbol myristate acetate in vitro. P
rostaglandins are known to inhibit various responses of neutrophils to infl
ammatory stimuli. We could show that prostaglandins inhibit N-formyl-methio
nyl-leucyl-phenylalanine-induced up-regulation of CD66 on peripheral blood
PMN in a concentration-dependent manner.