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Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection

SaBio. Instituto de Investigación en Recursos Cinegéticos IREC (CSIC-UCLM-JCCM), Ciudad Real 13005, Spain
Center for Infection and Immunity of Lille (CIIL), INSERM U1019-CNRS UMR 8204, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59000, France
Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University, Stillwater, OK 74078, USA
Authors to whom correspondence should be addressed.
Academic Editor: Ulrike Munderloh
Vet. Sci. 2016, 3(3), 15;
Received: 30 May 2016 / Revised: 11 July 2016 / Accepted: 13 July 2016 / Published: 15 July 2016
(This article belongs to the Special Issue Comparative Studies in Tick-Borne Diseases in Animals and Humans)
Anaplasma phagocytophilum is an emerging zoonotic pathogen that causes human and animal granulocytic anaplasmosis and tick-borne fever of ruminants. This obligate intracellular bacterium evolved to use common strategies to establish infection in both vertebrate hosts and tick vectors. Herein, we discuss the different strategies used by the pathogen to modulate cell apoptosis and establish infection in host cells. In vertebrate neutrophils and human promyelocytic cells HL-60, both pro-apoptotic and anti-apoptotic factors have been reported. Tissue-specific differences in tick response to infection and differential regulation of apoptosis pathways have been observed in adult female midguts and salivary glands in response to infection with A. phagocytophilum. In tick midguts, pathogen inhibits apoptosis through the Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway, while in salivary glands, the intrinsic apoptosis pathways is inhibited but tick cells respond with the activation of the extrinsic apoptosis pathway. In Ixodes scapularis ISE6 cells, bacterial infection down-regulates mitochondrial porin and manipulates protein processing in the endoplasmic reticulum and cell glucose metabolism to inhibit apoptosis and facilitate infection, whereas in IRE/CTVM20 tick cells, inhibition of apoptosis appears to be regulated by lower caspase levels. These results suggest that A. phagocytophilum uses different mechanisms to inhibit apoptosis for infection of both vertebrate and invertebrate hosts. View Full-Text
Keywords: tick; Anaplasma; apoptosis; neutrophil; immunology; tick-borne diseases; Ixodes tick; Anaplasma; apoptosis; neutrophil; immunology; tick-borne diseases; Ixodes
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MDPI and ACS Style

Alberdi, P.; Espinosa, P.J.; Cabezas-Cruz, A.; De la Fuente, J. Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection. Vet. Sci. 2016, 3, 15.

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