<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms

Non-tuberculosis mycobacteria (NTM) are ubiquitously found throughout the environment. NTM can cause respiratory infections in individuals with underlying lung conditions when inhaled, or systemic infections when ingested by patients with impaired immune systems. Current therapies can be ineffective...

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Autores principales:	Norah Abukhalid, Sabrina Islam, Robert Ndzeidze, Luiz E. Bermudez
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	<i>Mycobacterium avium</i> subspecies <i>hominissuis</i> nitric oxide host-pathogen interface amoeba and macrophage reactive oxidative radicals Medicine R
Acceso en línea:	https://doaj.org/article/a85ae387788f476093c0982b1f1323a0
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spelling	oai:doaj.org-article:a85ae387788f476093c0982b1f1323a02021-11-25T18:37:39Z<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms10.3390/pathogens101113652076-0817https://doaj.org/article/a85ae387788f476093c0982b1f1323a02021-10-01T00:00:00Zhttps://www.mdpi.com/2076-0817/10/11/1365https://doaj.org/toc/2076-0817Non-tuberculosis mycobacteria (NTM) are ubiquitously found throughout the environment. NTM can cause respiratory infections in individuals with underlying lung conditions when inhaled, or systemic infections when ingested by patients with impaired immune systems. Current therapies can be ineffective at treating NTM respiratory infections, even after a long course or with multidrug treatment regimens. NTM, such as <i>Mycobacterium avium</i> subspecies <i>hominissuis</i> (<i>M. avium</i>), is an opportunistic pathogen that shares environments with ubiquitous free-living amoeba and other environmental hosts, possibly their evolutionary hosts. It is highly likely that interactions between <i>M. avium</i> and free-living amoeba have provided selective pressure on the bacteria to acquire survival mechanisms, which are also used against predation by macrophages. In macrophages, <i>M. avium</i> resides inside phagosomes and has been shown to exit it to infect other cells. <i>M. avium’s</i> adaptation to the hostile intra-phagosomal environment is due to many virulence mechanisms. <i>M. avium</i> is able to switch the phenotype of the macrophage to be anti-inflammatory (M2). Here, we have focused on and discussed the bacterial defense mechanisms associated with the intra-phagosome phase of infection. <i>M. avium</i> possesses a plethora of antioxidant enzymes, including the superoxide dismutases, catalase and alkyl hydroperoxide reductase. When these defenses fail or are overtaken by robust oxidative burst, many other enzymes exist to repair damage incurred on <i>M. avium</i> proteins, including thioredoxin/thioredoxin reductase. Finally, <i>M. avium</i> has several oxidant sensors that induce transcription of antioxidant enzymes, oxidation repair enzymes and biofilm- promoting genes. These expressions induce physiological changes that allow <i>M. avium</i> to survive in the face of leukocyte-generated oxidative stress. We will discuss the strategies used by <i>M. avium</i> to infect human macrophages that evolved during its evolution from free-living amoeba. The more insight we gain about <i>M. avium’s</i> mode of pathogenicity, the more targets we can have to direct new anti-virulence therapies toward.Norah AbukhalidSabrina IslamRobert NdzeidzeLuiz E. BermudezMDPI AGarticle<i>Mycobacterium avium</i> subspecies <i>hominissuis</i>nitric oxidehost-pathogen interfaceamoeba and macrophagereactive oxidative radicalsMedicineRENPathogens, Vol 10, Iss 1365, p 1365 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	<i>Mycobacterium avium</i> subspecies <i>hominissuis</i> nitric oxide host-pathogen interface amoeba and macrophage reactive oxidative radicals Medicine R
spellingShingle	<i>Mycobacterium avium</i> subspecies <i>hominissuis</i> nitric oxide host-pathogen interface amoeba and macrophage reactive oxidative radicals Medicine R Norah Abukhalid Sabrina Islam Robert Ndzeidze Luiz E. Bermudez <i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
description	Non-tuberculosis mycobacteria (NTM) are ubiquitously found throughout the environment. NTM can cause respiratory infections in individuals with underlying lung conditions when inhaled, or systemic infections when ingested by patients with impaired immune systems. Current therapies can be ineffective at treating NTM respiratory infections, even after a long course or with multidrug treatment regimens. NTM, such as <i>Mycobacterium avium</i> subspecies <i>hominissuis</i> (<i>M. avium</i>), is an opportunistic pathogen that shares environments with ubiquitous free-living amoeba and other environmental hosts, possibly their evolutionary hosts. It is highly likely that interactions between <i>M. avium</i> and free-living amoeba have provided selective pressure on the bacteria to acquire survival mechanisms, which are also used against predation by macrophages. In macrophages, <i>M. avium</i> resides inside phagosomes and has been shown to exit it to infect other cells. <i>M. avium’s</i> adaptation to the hostile intra-phagosomal environment is due to many virulence mechanisms. <i>M. avium</i> is able to switch the phenotype of the macrophage to be anti-inflammatory (M2). Here, we have focused on and discussed the bacterial defense mechanisms associated with the intra-phagosome phase of infection. <i>M. avium</i> possesses a plethora of antioxidant enzymes, including the superoxide dismutases, catalase and alkyl hydroperoxide reductase. When these defenses fail or are overtaken by robust oxidative burst, many other enzymes exist to repair damage incurred on <i>M. avium</i> proteins, including thioredoxin/thioredoxin reductase. Finally, <i>M. avium</i> has several oxidant sensors that induce transcription of antioxidant enzymes, oxidation repair enzymes and biofilm- promoting genes. These expressions induce physiological changes that allow <i>M. avium</i> to survive in the face of leukocyte-generated oxidative stress. We will discuss the strategies used by <i>M. avium</i> to infect human macrophages that evolved during its evolution from free-living amoeba. The more insight we gain about <i>M. avium’s</i> mode of pathogenicity, the more targets we can have to direct new anti-virulence therapies toward.
format	article
author	Norah Abukhalid Sabrina Islam Robert Ndzeidze Luiz E. Bermudez
author_facet	Norah Abukhalid Sabrina Islam Robert Ndzeidze Luiz E. Bermudez
author_sort	Norah Abukhalid
title	<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
title_short	<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
title_full	<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
title_fullStr	<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
title_full_unstemmed	<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms
title_sort	<i>mycobacterium avium</i> subsp. <i>hominissuis</i> interactions with macrophage killing mechanisms
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/a85ae387788f476093c0982b1f1323a0
work_keys_str_mv	AT norahabukhalid imycobacteriumaviumisubspihominissuisiinteractionswithmacrophagekillingmechanisms AT sabrinaislam imycobacteriumaviumisubspihominissuisiinteractionswithmacrophagekillingmechanisms AT robertndzeidze imycobacteriumaviumisubspihominissuisiinteractionswithmacrophagekillingmechanisms AT luizebermudez imycobacteriumaviumisubspihominissuisiinteractionswithmacrophagekillingmechanisms
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<i>Mycobacterium avium</i> Subsp. <i>hominissuis</i> Interactions with Macrophage Killing Mechanisms

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