Peritonitis induces rat cardiac myocytes to promote polymorphonuclear leukocyte emigration and activate endothelial cells: Effect of lipopolysaccharide pretreatment
Peritonitis induces rat cardiac myocytes to promote polymorphonuclear leukocyte emigration and activate endothelial cells: Effect of lipopolysaccharide pretreatment
复制标题
腹膜炎诱导大鼠心肌细胞促进多形核白细胞迁移并激活内皮细胞：脂多糖预处理的作用
作者：
W. S. Madorin;G. Cepinskas;P. Kvietys
盲肠结扎和穿孔引起的腹膜炎导致大鼠心肌的炎症和功能障碍，心肌是远离感染部位的器官。这种腹膜炎诱导的病理可以通过在盲肠结扎和穿孔之前用脂多糖预处理这些动物来预防。在本研究中，我们评估了a）从盲肠结扎和穿孔大鼠中获得的心肌细胞是否可以诱导多形核白细胞跨内皮迁移，B）这些心肌细胞是否可以激活内皮细胞（增加促粘附表型），以及c）这些反应是否可以通过脂多糖预处理减弱。设计前瞻性动物研究。设置实验动物实验室。受试者：雄性Sprague道利大鼠。干预脂多糖预处理和未预处理的大鼠进行盲肠结扎和穿孔或剖腹手术。手术后6小时分离肌细胞并用于体外实验。测量和主要结果从盲肠结扎和穿孔大鼠分离的肌细胞促进多形核白细胞迁移通过大鼠内皮细胞单层，血小板活化因子受体拮抗剂防止的效果。从这些动物中分离的肌细胞也增加了大鼠内皮细胞上细胞间粘附分子-1的表面水平表达，这种作用也被血小板活化因子受体拮抗剂阻止。从用脂多糖预处理然后进行盲肠结扎和穿孔的大鼠中分离的肌细胞没有a）促进多形核白细胞跨内皮迁移或B）增加内皮细胞上的细胞间粘附分子-1表面表达。结论我们的研究结果表明，腹膜炎的诱导导致全身反应，诱导心肌细胞成为促炎性细胞（即，这些肌细胞产生趋化因子并激活内皮细胞）。盲肠结扎和穿孔的这种作用通过在诱导腹膜炎之前用脂多糖预处理动物而消除。
ObjectivePeritonitis induced by cecal ligation and perforation results in inflammation and dysfunction of the rat myocardium, an organ remote from the locus of infection. This peritonitis-induced pathology can be prevented by pretreating these animals with lipopolysaccharide before cecal ligation and perforation. In the present study, we assessed a) whether cardiomyocytes obtained from rats subjected to cecal ligation and perforation could induce polymorphonuclear leukocyte transendothelial migration, b) whether these cardiomyocytes could activate endothelial cells (increased proadhesive phenotype), and c) whether these responses could be attenuated by lipopolysaccharide pretreatment. DesignProspective animal study. SettingExperimental animal laboratory. SubjectsMale Sprague Dawley rats. InterventionsLipopolysaccharide pretreated and nonpretreated rats were subjected to cecal ligation and perforation or to laparotomy. Myocytes were isolated 6 hrs after surgery and used for in vitro experiments. Measurements and Main Results Myocytes isolated from cecal ligation and perforation rats promoted migration of polymorphonuclear leukocytes across a rat endothelial cell monolayer, an effect prevented by platelet activating factor receptor antagonists. Myocytes isolated from these animals also increased surface level expression of intercellular adhesion molecule-1 on rat endothelial cells, an effect also prevented by platelet activating factor receptor antagonists. Myocytes isolated from rats pretreated with lipopolysaccharide and then subjected to cecal ligation and perforation did not a) promote polymorphonuclear leukocyte transendothelial migration or b) increase intercellular adhesion molecule-1 surface expression on endothelial cells. ConclusionsOur findings indicate that induction of peritonitis results in a systemic response that induces cardiac myocytes to become proinflammatory (i.e., these myocytes produce chemotactic factors and activate endothelial cells). This effect of cecal ligation and perforation is abrogated by pretreating animals with lipopolysaccharide before induction of peritonitis.
消化酶的去热原降低了离体心肌细胞的脂多糖耐受性。
DOI：
10.1006/jmcc.1997.0432
发表时间：
1997
期刊：
Journal of molecular and cellular cardiology.
影响因子：
--
作者：
Lew,WY;Lee,M;Yasuda,S;Bayna,E
通讯作者：
Bayna,E
中性粒细胞粘附于内皮细胞。
DOI：
--
发表时间：
1993
期刊：
Blood cells
影响因子：
--
作者：
Abbassi,O;Kishimoto,TK;McIntire,LV;Smith,CW
通讯作者：
Smith,CW
影响因子：
15.9
作者：
ENTMAN, ML;YOUKER, K;SMITH, CW
通讯作者：
SMITH, CW