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Monocyte-platelet interaction induces a pro-inflammatory phenotype in circulating monocytes.
PLoS One. 2011; 6(10):e25595.Plos

Abstract

BACKGROUND

Activated platelets exert a pro-inflammatory action that can be largely ascribed to their ability to interact with leukocytes and modulate their activity. We hypothesized that platelet activation and consequent formation of monocyte-platelet aggregates (MPA) induces a pro-inflammatory phenotype in circulating monocytes.

METHODOLOGY/PRINCIPAL FINDINGS

CD62P(+) platelets and MPA were measured, and monocytes characterized, by whole blood flow cytometry in healthy subjects, before and two days after receiving influenza immunization. Three monocytic subsets were identified: CD14(+)CD16(-), CD14(high)CD16(+)and CD14(low)CD16(+). The increase in high sensitivity C-reactive protein post-immunization was accompanied by increased platelet activation and MPA formation (25.02±12.57 vs 41.48±16.81; p = 0.01), along with enhancement of circulating CD14(high)CD16(+) cells (4.7±3.6 vs 10.4±4.8; p = 0.003), their percentage being linearly related to levels of CD62P(+)-platelets (r(2) = 0.4347; p = 0.0008). In separate in vitro experiments, co-incubation of CD14(+)CD16(-) cells, isolated from healthy donor subjects, with autologous platelets gave rise to up-regulation of CD16 on monocytes as compared with those maintained in medium alone (% change in CD14(+)CD16(+) cells following 48 h co-incubation of monocytes with platelets was +106±51% vs monocytes in medium alone; p<0.001). This effect correlated directly with degree of MPA formation (r(2) = 0.7731; p<0.0001) and was associated with increased monocyte adhesion to endothelial cells. P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809.

CONCLUSIONS/SIGNIFICANCE

These data suggest that MPA formation, as occurs in the blood under pro-inflammatory conditions, expands the pool of circulating CD14(high)CD16(+) monocytes in a COX-2 dependent manner, and these monocytes exhibit increased adhesion to endothelium. Our findings delineate a novel mechanism underlying the pro-inflammatory effect of platelet activation.

Authors+Show Affiliations

Cardiovascular Division, Department of Clinical Pharmacology, King's College London, London, United Kingdom.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22022418

Citation

Passacquale, Gabriella, et al. "Monocyte-platelet Interaction Induces a Pro-inflammatory Phenotype in Circulating Monocytes." PloS One, vol. 6, no. 10, 2011, pp. e25595.
Passacquale G, Vamadevan P, Pereira L, et al. Monocyte-platelet interaction induces a pro-inflammatory phenotype in circulating monocytes. PLoS ONE. 2011;6(10):e25595.
Passacquale, G., Vamadevan, P., Pereira, L., Hamid, C., Corrigall, V., & Ferro, A. (2011). Monocyte-platelet interaction induces a pro-inflammatory phenotype in circulating monocytes. PloS One, 6(10), e25595. https://doi.org/10.1371/journal.pone.0025595
Passacquale G, et al. Monocyte-platelet Interaction Induces a Pro-inflammatory Phenotype in Circulating Monocytes. PLoS ONE. 2011;6(10):e25595. PubMed PMID: 22022418.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Monocyte-platelet interaction induces a pro-inflammatory phenotype in circulating monocytes. AU - Passacquale,Gabriella, AU - Vamadevan,Padman, AU - Pereira,Luis, AU - Hamid,Colleen, AU - Corrigall,Valerie, AU - Ferro,Albert, Y1 - 2011/10/12/ PY - 2011/07/26/received PY - 2011/09/06/accepted PY - 2011/10/25/entrez PY - 2011/10/25/pubmed PY - 2012/2/18/medline SP - e25595 EP - e25595 JF - PloS one JO - PLoS ONE VL - 6 IS - 10 N2 - BACKGROUND: Activated platelets exert a pro-inflammatory action that can be largely ascribed to their ability to interact with leukocytes and modulate their activity. We hypothesized that platelet activation and consequent formation of monocyte-platelet aggregates (MPA) induces a pro-inflammatory phenotype in circulating monocytes. METHODOLOGY/PRINCIPAL FINDINGS: CD62P(+) platelets and MPA were measured, and monocytes characterized, by whole blood flow cytometry in healthy subjects, before and two days after receiving influenza immunization. Three monocytic subsets were identified: CD14(+)CD16(-), CD14(high)CD16(+)and CD14(low)CD16(+). The increase in high sensitivity C-reactive protein post-immunization was accompanied by increased platelet activation and MPA formation (25.02±12.57 vs 41.48±16.81; p = 0.01), along with enhancement of circulating CD14(high)CD16(+) cells (4.7±3.6 vs 10.4±4.8; p = 0.003), their percentage being linearly related to levels of CD62P(+)-platelets (r(2) = 0.4347; p = 0.0008). In separate in vitro experiments, co-incubation of CD14(+)CD16(-) cells, isolated from healthy donor subjects, with autologous platelets gave rise to up-regulation of CD16 on monocytes as compared with those maintained in medium alone (% change in CD14(+)CD16(+) cells following 48 h co-incubation of monocytes with platelets was +106±51% vs monocytes in medium alone; p<0.001). This effect correlated directly with degree of MPA formation (r(2) = 0.7731; p<0.0001) and was associated with increased monocyte adhesion to endothelial cells. P-selectin glycoprotein ligand-1 (PSGL-1) blocking antibody, which abrogates MPA formation, abolished these effects, as did the cyclooxygenase (COX)-2 selective inhibitor NS-398, aspirin and the EP1/EP2-selective antagonist AH6809. CONCLUSIONS/SIGNIFICANCE: These data suggest that MPA formation, as occurs in the blood under pro-inflammatory conditions, expands the pool of circulating CD14(high)CD16(+) monocytes in a COX-2 dependent manner, and these monocytes exhibit increased adhesion to endothelium. Our findings delineate a novel mechanism underlying the pro-inflammatory effect of platelet activation. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/22022418/Monocyte_platelet_interaction_induces_a_pro_inflammatory_phenotype_in_circulating_monocytes_ L2 - http://dx.plos.org/10.1371/journal.pone.0025595 DB - PRIME DP - Unbound Medicine ER -