Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection
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 dis...
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MDPI AG
2016-07-01
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Online Access: | http://www.mdpi.com/2306-7381/3/3/15 |
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author | Pilar Alberdi Pedro J. Espinosa Alejandro Cabezas-Cruz José de la Fuente |
author_facet | Pilar Alberdi Pedro J. Espinosa Alejandro Cabezas-Cruz José de la Fuente |
author_sort | Pilar Alberdi |
collection | DOAJ |
description | 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. |
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issn | 2306-7381 |
language | English |
last_indexed | 2024-12-23T23:46:08Z |
publishDate | 2016-07-01 |
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spelling | doaj.art-68d91e6ca7664fdcb5a052d54463abab2022-12-21T17:25:31ZengMDPI AGVeterinary Sciences2306-73812016-07-01331510.3390/vetsci3030015vetsci3030015Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish InfectionPilar Alberdi0Pedro J. Espinosa1Alejandro Cabezas-Cruz2José de la Fuente3SaBio. Instituto de Investigación en Recursos Cinegéticos IREC (CSIC-UCLM-JCCM), Ciudad Real 13005, SpainSaBio. Instituto de Investigación en Recursos Cinegéticos IREC (CSIC-UCLM-JCCM), Ciudad Real 13005, SpainCenter for Infection and Immunity of Lille (CIIL), INSERM U1019-CNRS UMR 8204, Université Lille Nord de France, Institut Pasteur de Lille, Lille 59000, FranceSaBio. Instituto de Investigación en Recursos Cinegéticos IREC (CSIC-UCLM-JCCM), Ciudad Real 13005, SpainAnaplasma 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.http://www.mdpi.com/2306-7381/3/3/15tickAnaplasmaapoptosisneutrophilimmunologytick-borne diseasesIxodes |
spellingShingle | Pilar Alberdi Pedro J. Espinosa Alejandro Cabezas-Cruz José de la Fuente Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection Veterinary Sciences tick Anaplasma apoptosis neutrophil immunology tick-borne diseases Ixodes |
title | Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection |
title_full | Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection |
title_fullStr | Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection |
title_full_unstemmed | Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection |
title_short | Anaplasma phagocytophilum Manipulates Host Cell Apoptosis by Different Mechanisms to Establish Infection |
title_sort | anaplasma phagocytophilum manipulates host cell apoptosis by different mechanisms to establish infection |
topic | tick Anaplasma apoptosis neutrophil immunology tick-borne diseases Ixodes |
url | http://www.mdpi.com/2306-7381/3/3/15 |
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