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血营养支原体可诱导红细胞发生程序性细胞死亡。

Hemotrophic mycoplasmas induce programmed cell death in red blood cells.

作者信息

Felder Kathrin M, Hoelzle Katharina, Ritzmann Mathias, Kilchling Tim, Schiele Daniela, Heinritzi Karl, Groebel Katrin, Hoelzle Ludwig E

机构信息

Institute of Veterinary Bacteriology, Vetsuisse Faculty, University of Zurich, Zurich, Switzerland.

出版信息

Cell Physiol Biochem. 2011;27(5):557-64. doi: 10.1159/000329957. Epub 2011 Jun 15.

DOI:10.1159/000329957
PMID:21691073
Abstract

Hemotrophic mycoplasmas (HM) are uncultivable bacteria found on and in the red blood cells (RBCs). The main clinical sign of HM infections is the hemolytic anemia. However, anemia-inducing pathogenesis has not been totally clarified. In this work we used the splenectomized pig as animal model and Mycoplasma suis as a representative for hemotrophic mycoplasmas to study anemia pathogenesis. Eryptosis, i.e. programmed cell death of RBCs, is characterized by cell shrinkage, microvesiculation and phosphatidylserine (PS) exposure on the outer membrane. The eryptosis occurrence and its influence on anemia pathogenesis was observed over the time-course of M. suis infections in pigs using 3 M. suis isolates of differing virulence. All 3 isolates induced eryptosis, but with different characteristics. The occurrence of eryptosis could as well be confirmed in vitro: serum and plasma of an acutely ill pig induced PS exposure on erythrocytes drawn from healthy pigs. Since M. suis is able to induce eryptotic processes it is concluded that eryptosis is one anemia-inducing factor during M. suis infections and, therefore, plays a significant role in the pathogenesis of infectious anemia due to HM infection.

摘要

血营养支原体(HM)是存在于红细胞(RBC)表面及内部的不可培养细菌。HM感染的主要临床症状是溶血性贫血。然而,导致贫血的发病机制尚未完全阐明。在本研究中,我们以脾切除猪作为动物模型,以猪支原体作为血营养支原体的代表,来研究贫血的发病机制。红细胞凋亡,即红细胞的程序性细胞死亡,其特征为细胞皱缩、微囊泡形成以及外膜上磷脂酰丝氨酸(PS)暴露。使用3株毒力不同的猪支原体分离株,在猪感染猪支原体的时间进程中观察红细胞凋亡的发生及其对贫血发病机制的影响。所有3株分离株均诱导红细胞凋亡,但具有不同特征。红细胞凋亡的发生在体外也得到证实:急性病猪的血清和血浆可诱导从健康猪采集的红细胞发生PS暴露。由于猪支原体能够诱导红细胞凋亡过程,因此得出结论,红细胞凋亡是猪支原体感染期间导致贫血的一个因素,因此在HM感染所致传染性贫血的发病机制中起重要作用。

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