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

Authors: Perretti, M  Wheller, SK  Flower, RJ  Wahid, S  Pitzalis, C 
Citation: Perretti M, etal., J Leukoc Biol. 1999 May;65(5):583-9.
Pubmed: (View Article at PubMed) PMID:10331485

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.


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CRRD Object Information
CRRD ID: 7421575
Created: 2013-11-21
Species: All species
Last Modified: 2013-11-21
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.