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 (approximately 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.
Perretti
M
M
Department of Biochemical Pharmacology, The William Harvey Research Institute, London, United Kingdom. m.perretti@qmw.ac.uk
Wheller
S K
SK
Flower
R J
RJ
Wahid
S
S
Pitzalis
C
C
D000328:Adult; D017305:Annexin A1 / Q000097:blood / Q000378:metabolism*; D001768:Blister / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D002448:Cell Adhesion / Q000276:immunology; D002465:Cell Movement / Q000276:immunology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D006801:Humans; D006968:Hypersensitivity, Delayed / Q000276:immunology* / Q000473:pathology; D007963:Leukocytes, Mononuclear / Q000276:immunology / Q000378:metabolism*; D012867:Skin / Q000276:immunology* / Q000473:pathology
D017305:Annexin A1