Rollo Ellen E, Hempson Scott J, Bansal Ajay, Tsao Ernest, Habib Iman, Rittling Susan R, Denhardt David T, Mackow Erich R, Shaw Robert D
Research Service (151), Northport V.A. Medical Center, Northport, NY 11768, USA.
J Virol. 2005 Mar;79(6):3509-16. doi: 10.1128/JVI.79.6.3509-3516.2005.
Osteopontin (OPN) is a sialated phosphoprotein found in tissues and secreted into body fluids. It is an integrin ligand with pleiotropic functions as an extracellular matrix protein in mineralized tissues and a cytokine that is active in cell signaling (A. B. Tuck, C. Hota, S. M. Wilson, and A. F. Chambers, Oncogene 22:1198-1205, 2003). To determine whether OPN may be important in mucosal defense against viral pathogens, we evaluated the OPN response to rotavirus infection and the extent of diarrhea manifested by infected opn null mutant (opn-/-) mice. Reverse transcription-PCR, Northern and Western blots, and immunohistochemical studies of the HT-29 intestinal epithelial cell line and murine intestine were used to evaluate OPN mRNA and product. Intestinal closed loops and diarrheal observations determined disease severity and duration. OPN mRNA levels increased after infection of HT-29 cells, peaking in 4 to 6 h. Infected cultures contained 925 microg of OPN/ml, while for controls the levels were below detection (50 microg/ml). Infection increased OPN mRNA levels in intestinal tissue between 2 and 24 h postinoculation and increased OPN protein in intestinal fluid. The cellular localization of OPN was supranuclear and apical, and responding cells were diffusely distributed on the villus surface. Three days after infection, closed intestinal loops from opn-/- mice contained more fluid than loops from controls, although secretion levels at the onset of illness were similar. Null mutant mice experienced more intense and prolonged diarrhea than controls. Rotavirus infection of intestinal epithelial cells and murine intestine caused marked increases in OPN mRNA levels and secreted OPN protein. OPN-deficient mice suffered prolonged disease.
骨桥蛋白(OPN)是一种在组织中发现并分泌到体液中的唾液酸化磷蛋白。它是一种整合素配体,作为矿化组织中的细胞外基质蛋白具有多效性功能,也是一种在细胞信号传导中起作用的细胞因子(A. B. 塔克、C. 霍塔、S. M. 威尔逊和A. F. 钱伯斯,《癌基因》22:1198 - 1205,2003年)。为了确定OPN在黏膜抵御病毒病原体方面是否重要,我们评估了OPN对轮状病毒感染的反应以及感染opn基因敲除突变体(opn-/-)小鼠出现腹泻的程度。使用HT - 29肠上皮细胞系和小鼠肠道的逆转录 - PCR、Northern和Western印迹以及免疫组织化学研究来评估OPN mRNA和产物。肠道封闭肠袢和腹泻观察确定了疾病的严重程度和持续时间。HT - 29细胞感染后OPN mRNA水平升高,在4至6小时达到峰值。感染的培养物中OPN含量为925微克/毫升,而对照水平低于检测限(50微克/毫升)。接种后2至24小时内,感染使肠道组织中的OPN mRNA水平升高,肠液中的OPN蛋白增加。OPN的细胞定位在核上和顶端,反应细胞在绒毛表面呈弥漫性分布。感染三天后,opn-/-小鼠的封闭肠袢比对照的含有更多液体,尽管发病初期的分泌水平相似。基因敲除突变体小鼠比对照经历更剧烈和持续时间更长的腹泻。肠道上皮细胞和小鼠肠道的轮状病毒感染导致OPN mRNA水平和分泌的OPN蛋白显著增加。缺乏OPN的小鼠患病时间延长。