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Immune Evasion of Mycoplasma bovis

Mycoplasma bovis (M. bovis) causes various chronic inflammatory diseases, including mastitis and bronchopneumonia, in dairy and feed cattle. It has been found to suppress the host immune response during infection, leading to the development of chronic conditions. Both in vitro and in vivo studies ha...

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Autores principales: Askar, Hussam, Chen, Shengli, Hao, Huafang, Yan, Xinmin, Ma, Lina, Liu, Yongsheng, Chu, Yuefeng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7998117/
https://www.ncbi.nlm.nih.gov/pubmed/33806506
http://dx.doi.org/10.3390/pathogens10030297
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author Askar, Hussam
Chen, Shengli
Hao, Huafang
Yan, Xinmin
Ma, Lina
Liu, Yongsheng
Chu, Yuefeng
author_facet Askar, Hussam
Chen, Shengli
Hao, Huafang
Yan, Xinmin
Ma, Lina
Liu, Yongsheng
Chu, Yuefeng
author_sort Askar, Hussam
collection PubMed
description Mycoplasma bovis (M. bovis) causes various chronic inflammatory diseases, including mastitis and bronchopneumonia, in dairy and feed cattle. It has been found to suppress the host immune response during infection, leading to the development of chronic conditions. Both in vitro and in vivo studies have confirmed that M. bovis can induce proinflammatory cytokines and chemokines in the host. This consists of an inflammatory response in the host that causes pathological immune damage, which is essential for the pathogenic mechanism of M. bovis. Additionally, M. bovis can escape host immune system elimination and, thus, cause chronic infection. This is accomplished by preventing phagocytosis and inhibiting key responses, including the neutrophil respiratory burst and the development of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) that lead to the creation of an extracellular bactericidal network, in addition to inhibiting monocyte and alveolar macrophage apoptosis and inducing monocytes to produce anti-inflammatory factors, thus inducing the apoptosis of peripheral blood mononuclear cells (PBMCs), inhibiting their proliferative response and resulting in their invasion. Together, these conditions lead to long-term M. bovis infection. In terms of the pathogenic mechanism, M. bovis may invade specific T-cell subsets and induce host generation of exhausted T-cells, which helps it to escape immune clearance. Moreover, the M. bovis antigen exhibits high-frequency variation in size and expression period, which allows it to avoid activation of the host humoral immune response. This review includes some recent advances in studying the immune response to M. bovis. These may help to further understand the host immune response against M. bovis and to develop potential therapeutic approaches to control M. bovis infection.
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spelling pubmed-79981172021-03-28 Immune Evasion of Mycoplasma bovis Askar, Hussam Chen, Shengli Hao, Huafang Yan, Xinmin Ma, Lina Liu, Yongsheng Chu, Yuefeng Pathogens Review Mycoplasma bovis (M. bovis) causes various chronic inflammatory diseases, including mastitis and bronchopneumonia, in dairy and feed cattle. It has been found to suppress the host immune response during infection, leading to the development of chronic conditions. Both in vitro and in vivo studies have confirmed that M. bovis can induce proinflammatory cytokines and chemokines in the host. This consists of an inflammatory response in the host that causes pathological immune damage, which is essential for the pathogenic mechanism of M. bovis. Additionally, M. bovis can escape host immune system elimination and, thus, cause chronic infection. This is accomplished by preventing phagocytosis and inhibiting key responses, including the neutrophil respiratory burst and the development of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) that lead to the creation of an extracellular bactericidal network, in addition to inhibiting monocyte and alveolar macrophage apoptosis and inducing monocytes to produce anti-inflammatory factors, thus inducing the apoptosis of peripheral blood mononuclear cells (PBMCs), inhibiting their proliferative response and resulting in their invasion. Together, these conditions lead to long-term M. bovis infection. In terms of the pathogenic mechanism, M. bovis may invade specific T-cell subsets and induce host generation of exhausted T-cells, which helps it to escape immune clearance. Moreover, the M. bovis antigen exhibits high-frequency variation in size and expression period, which allows it to avoid activation of the host humoral immune response. This review includes some recent advances in studying the immune response to M. bovis. These may help to further understand the host immune response against M. bovis and to develop potential therapeutic approaches to control M. bovis infection. MDPI 2021-03-04 /pmc/articles/PMC7998117/ /pubmed/33806506 http://dx.doi.org/10.3390/pathogens10030297 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Askar, Hussam
Chen, Shengli
Hao, Huafang
Yan, Xinmin
Ma, Lina
Liu, Yongsheng
Chu, Yuefeng
Immune Evasion of Mycoplasma bovis
title Immune Evasion of Mycoplasma bovis
title_full Immune Evasion of Mycoplasma bovis
title_fullStr Immune Evasion of Mycoplasma bovis
title_full_unstemmed Immune Evasion of Mycoplasma bovis
title_short Immune Evasion of Mycoplasma bovis
title_sort immune evasion of mycoplasma bovis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7998117/
https://www.ncbi.nlm.nih.gov/pubmed/33806506
http://dx.doi.org/10.3390/pathogens10030297
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