Jepson M A, Schlecht H B, Collares-Buzato C B
Cell Imaging Facility and Department of Biochemistry, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, United Kingdom.
Infect Immun. 2000 Dec;68(12):7202-8. doi: 10.1128/IAI.68.12.7202-7208.2000.
Infection of polarized MDCK epithelial layers by Salmonella enterica serovar Typhimurium is accompanied by increased tight junction permeability and by contraction of perijunctional actinomyosin. We localized dysfunctional tight junctions in serovar Typhimurium-infected MDCK layers by imaging apical-basolateral intramembrane diffusion of fluorescent lipid and found that loss of the apical-basolateral diffusion barrier (tight junction fence function) was most marked in areas of prominent perijunctional contraction. The protein kinase inhibitor staurosporine prevented perijunctional contraction but did not reverse the effects of serovar Typhimurium on tight junction barrier function. Hence, perijunctional contraction is not required for Salmonella-induced tight junction dysfunction and this epithelial response to infection may be multifactorial.
鼠伤寒沙门氏菌感染极化的MDCK上皮层会伴随着紧密连接通透性增加以及连接周围肌动球蛋白收缩。我们通过对荧光脂质的顶-基底膜内扩散进行成像,定位了鼠伤寒沙门氏菌感染的MDCK层中功能失调的紧密连接,发现顶-基底扩散屏障(紧密连接围栏功能)的丧失在连接周围明显收缩的区域最为显著。蛋白激酶抑制剂星形孢菌素可防止连接周围收缩,但不能逆转鼠伤寒沙门氏菌对紧密连接屏障功能的影响。因此,连接周围收缩并非沙门氏菌诱导紧密连接功能障碍所必需,这种上皮对感染的反应可能是多因素的。