Innate immune tissue injury and murine HGA - Tissue injury in the murine model of granulocytic anaplasmosis relates to host innate immune response and not pathogen load

被引：12

作者：

Scorpio, Diana G.

Von Loewenich, Friederike D.

Bogdan, Christian

Dumler, J. Stephen

机构：

[1] Johns Hopkins Univ, Sch Med, Dept Comparat Med, Baltimore, MD 21205 USA

[2] Univ Freiburg, Inst Med Microbiol & Hyg, Freiburg, Germany

[3] Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA

来源：

RICKETTSIOSES: FROM GENOME TO PROTEOME, PATHOBIOLOGY, AND RICKETTSIAE AS AN INTERNATIONAL THREAT | 2005年 / 1063卷

关键词：

Anaplasma phagocytophilum; TNF; NOS2; phagocyte oxidase; innate immunity; mouse model;

D O I：

10.1196/annals.1355.077

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Anaplasma phagocytophilum is an obligate intracellular tick-borne bacterium that propagates within neutrophils and causes human and animal granulocytic anaplasmosis (HGA). In the murine model of HGA, host immune response plays a more important role in histopathologic lesions than does pathogen load. We examined the role of CYBB, NOS2, and TNF alpha as effectors of innate immune-related injury. Our hypothesis is that the innate immune response to A. phagocytophilum results in inflammatory histopathology, but does not control the pathogen.

引用

页码：425 / 428

页数：4

共 6 条

[1] Exploitation of interleukin-8-induced neutrophil chemotaxis by the agent of human granulocytic ehrlichiosis [J].