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.

Diana G. Scorpio; Friederike D. Von Loewenich; Christian Bogdan; J. Stephen Dumler

doi:10.1196/annals.1355.077

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.

Diana G. Scorpio^*
, Friederike D. Von Loewenich
, Christian Bogdan
, J. Stephen Dumler

^*Corresponding author for this work

Pathology

Research output: Contribution to journal › Article › peer-review

17 Scopus citations

Abstract

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 TNFalpha 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.

Original language	English
Pages (from-to)	425-428
Number of pages	4
Journal	Annals of the New York Academy of Sciences
Volume	1063
DOIs	https://doi.org/10.1196/annals.1355.077
State	Published - Dec 2005

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title = "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.",

abstract = "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 TNFalpha 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.",

author = "Scorpio, \{Diana G.\} and \{Von Loewenich\}, \{Friederike D.\} and Christian Bogdan and Dumler, \{J. Stephen\}",

year = "2005",

month = dec,

doi = "10.1196/annals.1355.077",

language = "English",

volume = "1063",

pages = "425--428",

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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. / Scorpio, Diana G.; Von Loewenich, Friederike D.; Bogdan, Christian et al.
In: Annals of the New York Academy of Sciences, Vol. 1063, 12.2005, p. 425-428.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Innate immune tissue injury and murine HGA

T2 - tissue injury in the murine model of granulocytic anaplasmosis relates to host innate immune response and not pathogen load.

AU - Scorpio, Diana G.

AU - Von Loewenich, Friederike D.

AU - Bogdan, Christian

AU - Dumler, J. Stephen

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N2 - 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 TNFalpha 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.

AB - 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 TNFalpha 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.

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DO - 10.1196/annals.1355.077

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JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

ER -

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.

Abstract

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