NDLI: Stat1 negatively regulates immune-mediated injury with Anaplasma phagocytophilum infection.

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Stat1 negatively regulates immune-mediated injury with Anaplasma phagocytophilum infection.

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Stat1 negatively regulates immune-mediated injury with Anaplasma phagocytophilum infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Dumler, J. Stephen Choi, Kyoung-Seong Scorpio, Diana G.
Description	Author Affiliation: Choi KS ( Department of Animal Biotechnology, College of Animal Science, Kyungpook National University, Sangju 742-711, Republic of Korea); Scorpio DG ( Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205); Dumler JS ( Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205)
Abstract	Human granulocytic anaplasmosis (HGA) is caused by the obligate intracellular bacterium Anaplasma phagocytophilum. Our data previously demonstrated that A. phagocytophilum induces an immunopathologic response by activating IFN-Î³ production through the Stat1 signaling pathway. In this study, we investigated the broader role of Stat1 signaling in the host response to infection with A. phagocytophilum. In Stat1 knockout (KO) compared with wild-type mice, A. phagocytophilum infection was more highly pathogenic as characterized by the unanticipated development of clinical signs in mice including markedly increased splenomegaly, more severe inflammatory splenic and hepatic histopathology, >100-fold higher blood and splenic bacterial loads, and more elevated proinflammatory cytokine/chemokine responses in serum. CD4(+) and CD8(+) T lymphocyte populations were significantly expanded in spleens of A. phagocytophilum-infected Stat1 KO mice compared with wild-type mice. The leukocyte infiltrates in the livers and spleens of A. phagocytophilum-infected Stat1 KO mice also contained expansions in neutrophil and monocyte/macrophage populations. Importantly, A. phagocytophilum-infected Stat1 KO mice did not demonstrate induction of inducible NO synthase in splenocytes. These results show that Stat1 plays an important role in controlling bacterial loads but also by unexpectedly providing an undefined mechanism for dampening of the immunopathologic response observed with A. phagocytophilum infection.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1401381
Journal	The Journal of Immunology
Issue Number	10
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Anaplasma Phagocytophilum Immunology Anaplasmosis Liver Stat1 Transcription Factor Spleen Genetics Microbiology Pathology Animals Bacterial Load Cd4-positive T-lymphocytes Cd8-positive T-lymphocytes Gene Expression Immunomodulation Macrophages Mice Mice, Knockout Monocytes Neutrophils Nitric Oxide Synthase Type Ii Deficiency Severity Of Illness Index Signal Transduction Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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