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Modulation of cellular annexin I in human leukocytes infiltrating DTH skin reactions

Based on our previous studies showing 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 (PBMC) were modified after adhesion to endothelial monolayers in vitro and extravasation into skin blisters in vivo. In vitro, annexin I levels were depleted more significantly (–70%) in post‐adherent PMNs than in monocytes (–25%) and lymphocytes (–50%, only in the positive fraction). In vivo, a significant time‐dependent increase (approximately threefold, P < 0.05) in cell‐associated annexin I was measured in PBMCs recovered from the blisters, whereas no significant changes were detected in extravasated PMNs. This was associated with annexin I release in the blister fluids (∼35 ng/mL), whereas no detectable protein was found in matched‐paired plasmas. In conclusion, we report for the first time an activation of the annexin I pathway during an ongoing experimental inflammatory response in humans, which is differently regulated between PMNs and PBMCs. J. Leukoc. Biol. 65: 583–589; 1999.