2023
DOI: 10.3389/fmicb.2023.983299
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Role of phagocyte extracellular traps during Mycobacterium tuberculosis infections and tuberculosis disease processes

Abstract: Mycobacterium tuberculosis (M.tb) infections remain one of the most significant causes of mortality worldwide. The current situation shows an emergence of new antibiotic-resistant strains making it difficult to control the tuberculosis (TB) disease. A large part of its success as a pathogen is due to its ability to persist for years or even decades without causing evident clinical manifestations. M.tb is highly successful in evading the host-defense by manipulating host-signalling pathways. Although macrophage… Show more

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Cited by 4 publications
(4 citation statements)
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“…It is assumed that mycobacteria activate the hyperproduction of ROS by neutrophils, provoking necrosis of immune cells, which ultimately weakens antimicrobial protection [48]. When triggering M. tuberculosisinfected neutrophil necrosis, ESAT-6 and CFP-10 proteins are responsible for stimulating the release of NETs [49]. Some authors consider the ability of M. tuberculosis to activate ROS-independent formation of METs by macrophages [49], in particular, the mycobacterial protein ESAT6 stimulated the formation of METs by human macrophages in in vitro studies [50].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…It is assumed that mycobacteria activate the hyperproduction of ROS by neutrophils, provoking necrosis of immune cells, which ultimately weakens antimicrobial protection [48]. When triggering M. tuberculosisinfected neutrophil necrosis, ESAT-6 and CFP-10 proteins are responsible for stimulating the release of NETs [49]. Some authors consider the ability of M. tuberculosis to activate ROS-independent formation of METs by macrophages [49], in particular, the mycobacterial protein ESAT6 stimulated the formation of METs by human macrophages in in vitro studies [50].…”
Section: Discussionmentioning
confidence: 99%
“…When triggering M. tuberculosisinfected neutrophil necrosis, ESAT-6 and CFP-10 proteins are responsible for stimulating the release of NETs [49]. Some authors consider the ability of M. tuberculosis to activate ROS-independent formation of METs by macrophages [49], in particular, the mycobacterial protein ESAT6 stimulated the formation of METs by human macrophages in in vitro studies [50]. The mycobacterial protein nucleoside diphosphate kinase (Ndk), which activates macrophage GTPases Rab5 and Rab7, reduced the formation of phagolysosomes by blocking the fusion of phagosomes and lysosomes [51].…”
Section: Discussionmentioning
confidence: 99%
“…While apoptosis of infected macrophages allows bacterial replication to be controlled and is subsequently associated with reduced pathogen viability, necrosis represents a mechanism that allows bacteria to evade host defenses and spread [ 65 , 71 ]. Infected macrophages secrete chemokines and cytokines that activate neutrophils, which in turn release reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) to kill M. tuberculosis [ 72 ]. To establish infection, M. tuberculosis inhibits ROS production by neutrophils which act as a niche for M. tuberculosis replication [ 72 ].…”
Section: Insights Into Pathogenesis Of Tuberculosismentioning
confidence: 99%
“…Infected macrophages secrete chemokines and cytokines that activate neutrophils, which in turn release reactive oxygen species (ROS) and neutrophil extracellular traps (NETs) to kill M. tuberculosis [ 72 ]. To establish infection, M. tuberculosis inhibits ROS production by neutrophils which act as a niche for M. tuberculosis replication [ 72 ]. At the same time, the bacilli activate a cascade of immune responses, recruiting DCs that phagocytize and transport M.tb to the draining lymph nodes to activate the T-cell-mediated immune response [ 73 ].…”
Section: Insights Into Pathogenesis Of Tuberculosismentioning
confidence: 99%