Based on our previous studies shelving endogenous annexin I being depleted
from migrated neutrophils (PMN) in vitro, we have tested whether the levels
of this glucocorticoid-regulated protein in PMN and mononuclear cells (PBM
C) were modified after adhesion to endothelial monolayers in vitro and extr
avasation into skin blisters in vivo. III vitro, annexin I levels were depl
eted more significantly (-70%) in post-adherent PMNs than bl monocytes (-25
%) and lymphocytes (-50%, only in the positive fraction), In vivo, a signif
icant time-dependent increase (approximately threefold, P < 0.05) in cell-a
ssociated annexin I tvas measured in PBMCs recovered from the blisters, whe
reas no significant changes were detected in extravasated PMNs, This,vas as
sociated with annexin I release in the blister fluids (similar to 35 ng/mL)
, whereas no detectable protein was found in matched-paired plasmas, In con
clusion, we report for the first time an activation of the annexin I pathwa
y during an ongoing experimental inflammatory response hi humans, which is
differently regulated between PMNs and PBMCs.