Coxsackievirus B₃affects endothelial tight junctions: Possible relationship to ZO‐1 and F‐actin, as well as p38 MAPK activity

Tight junction (TJ) plays a pivotal role in preventing the invasion of pathogens from the blood to extracellular environment. However, the mechanisms by which Group B coxsackievirus 3 (CVB(3)) can get through TJ from the apical surface still remain obscure. In the present study, the human umbilical vein endothelial cell (HUVEC) was utilized to investigate the alterations in F-actin and ZO-1 status, permeability as well as p38 mitogen-activated protein kinase (MAPK) activity in response to CVB(3) by means of fluorescence labeling, flow cytometry, and macromolecule permeability assay. We found that CVB(3) was able to induce reorganization of F-actin and redistribution of ZO-1, increase the level of F-actin, and elevate the permeability of FITC-albumin. Moreover, CVB(3)-mediated the above effects involve in P38 MAPK activation. Our preliminary study indicates that CVB(3)-induced alteration in permeability may be attributed to disruption of F-actin and ZO-1 organizations and that SB203580, a specific P38 MAPK inhibitor, can reverse these effects. The precise mechanisms underlying the CVB(3)-mediated effects on HUVECs need to be studied further.