PM2.5 and PM10 induce the expression of adhesion molecules and the adhesion of monocytic cells to human umbilical vein endothelial cells.
Exposure to airborne particles has been associated with an increase in cardiopulmonary events. Endothelial cells could be playing an important role in the response to airborne particles due their involvement in proinflammatory events, and there is some evidence of particle translocation from lung into circulation. One of the initiating events of inflammation is endothelial activation. We determined the concentration-response effect of a particulate matter with different aerodynamic sizes (PM2.5 [particulate matter with aerodynamic diameter of 2.5 microm and less] and PM10 [particulate matter with aerodynamic diameter of 10 microm and less]) obtained from Mexico City on human umbilical vein endothelial cells (HUVEC). The adhesion of monocytic U937 cells to HUVEC and the expression of early (E- and P-selectins) and late (ICAM-1, PECAM-1, VCAM-1) adhesion molecules were tested. Adhesion of U937 cells to HUVEC was evaluated by coculture experiments using [3H]thymidine-labeled U937 cells and the expression of adhesion molecules was evaluated by flow cytometry. Tumor necrosis factor (TNF)-alpha was used as a positive control of endothelial activation. Our results showed that both PM2.5 and PM10 induced the adhesion of U937 cells to HUVEC, and their maximal effect was observed at 20 microg/cm2. This adhesion was associated with an increase in the expression of all adhesion molecules evaluated for PM10, and E-selectin, P-selectin, and ICAM-1 for PM2.5. In general, maximum expression of adhesion molecules induced by PM2.5 and PM10 was obtained with 20 microg/cm2; however, PM10-induced expression was observed from 5 microg/cm2. E-selectin and ICAM-1 had the strongest expression in response to particles. In conclusion, PM2.5 and PM10 induce the activation of HUVEC, leading to monocytic adhesion via the expression of adhesion molecules, suggesting that these particles may participate in the development of inflammatory diseases. The role of these events in the development of diseases such as atherosclerosis is likely to be evaluated.
Montiel-Dávalos
Angélica
A
Department of Cell Biology, Instituto Nacional de Cardiología Ignacio Chávez, México.
Alfaro-Moreno
Ernesto
E
López-Marure
Rebeca
R
D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000096:biosynthesis*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D042783:Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D004730:Endothelium, Vascular / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D006801:Humans; D009000:Monocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D052638:Particulate Matter / Q000008:administration & dosage / Q000633:toxicity*; D020298:U937 Cells; D014471:Umbilical Veins / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism
D015815:Cell Adhesion Molecules; D052638:Particulate Matter