G protein-coupled receptor160 regulates mycobacteria entry into macrophages by activating ERK

Yang, Hua; Liu, Haipeng; Chen, Hao; Mo, Haiping; Chen, Jianxia; Huang, Xiaocheng; Zheng, Ruijuan; Z, Liu; Feng, Yonghong; Liu, Feng; Ge, Baoxue

doi:10.1016/j.cellsig.2016.05.022

Cited by 8 publications

(7 citation statements)

References 32 publications

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“…85,86 Interestingly, a recent study demonstrated that G protein-coupled receptor 160 (GPR160) regulates mycobacteria entry into macrophages by activating MAPK/ERK signaling, which suggests a crosstalk between the GPCR and TLR signaling pathways during mycobacterial infection. 87 Further in-depth studies of the underlying mechanisms of the interactions between TLR signaling pathways and Mtb components are warranted.…”

Section: Tlr Signalingmentioning

confidence: 99%

Innate immunity in tuberculosis: host defense vs pathogen evasion

2017

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The major innate immune cell types involved in tuberculosis (TB) infection are macrophages, dendritic cells (DCs), neutrophils and natural killer (NK) cells. These immune cells recognize the TB-causing pathogen Mycobacterium tuberculosis (Mtb) through various pattern recognition receptors (PRRs), including but not limited to Toll-like receptors (TLRs), Nod-like receptors (NLRs) and C-type lectin receptors (CLRs). Upon infection by Mtb, the host orchestrates multiple signaling cascades via the PRRs to launch a variety of innate immune defense functions such as phagocytosis, autophagy, apoptosis and inflammasome activation. In contrast, Mtb utilizes numerous exquisite strategies to evade or circumvent host innate immunity. Here we discuss recent research on major host innate immune cells, PRR signaling, and the cellular functions involved in Mtb infection, with a specific focus on the host's innate immune defense and Mtb immune evasion. A better understanding of the molecular mechanisms underlying host-pathogen interactions could provide a rational basis for the development of effective anti-TB therapeutics.

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Section: Tlr Signalingmentioning

confidence: 99%

Innate immunity in tuberculosis: host defense vs pathogen evasion

2017

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“…In addition, S1PR3 analog also increased p38/STAT3 phosphorylation, but no change in IL-6 secretion. On the other hand, ERK phosphorylation, which is essential for mycobacterial entry ( Yang et al, 2016 ) and enhanced IL-10 secretion following mycobacterial infection, which further blocks phagolysosome maturation for intracellular survival ( O'Leary et al, 2011 ). Previous clinical studies also revealed that increased IL-10 levels have been associated with active TB ( Gerosa et al, 1999 ; Verbon et al, 1999 ).…”

Section: Discussionmentioning

confidence: 99%

Sphingosine-1-phosphate receptors 2 and 3 reprogram resting human macrophages into M1 phenotype following mycobacteria infection

Arish

Naz

2022

Current Research in Immunology

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“…Previously, it was discovered that the M. tuberculosis -secreted proteins Mce3E and PtpA target MAPK and NF-κB pathways to modulate TLR signaling ( 75 , 76 ). Mycobacterial phagocytosis into macrophages was also promoted by activating the signaling pathways ERK and MAPK, which are likely to be involved in mycobacterial pathogenesis ( 77 ). More research is required to investigate the potential molecular interactions of TLR activating signaling pathways with M. tuberculosis receptors.…”

Section: Sars-cov-2 and M Tuberculosis Host Cellul...mentioning

confidence: 99%

Pathogenesis of SARS-CoV-2 and Mycobacterium tuberculosis Coinfection

Shah

Shah²,

Yasmeen³

et al. 2022

Front. Immunol.

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Coronavirus disease-2019 (COVID-19), caused by SARS-CoV-2, is an infectious disease that poses severe threats to global public health and significant economic losses. The COVID-19 global burden is rapidly increasing, with over 246.53 million COVID-19 cases and 49.97 million deaths reported in the WHO 2021 report. People with compromised immunity, such as tuberculosis (TB) patients, are highly exposed to severe COVID-19. Both COVID-19 and TB diseases spread primarily through respiratory droplets from an infected person to a healthy person, which may cause pneumonia and cytokine storms, leading to severe respiratory disorders. The COVID-19-TB coinfection could be fatal, exacerbating the current COVID-19 pandemic apart from cellular immune deficiency, coagulation activation, myocardial infarction, and other organ dysfunction. This study aimed to assess the pathogenesis of SARS-CoV-2-Mycobacterium tuberculosis coinfections. We provide a brief overview of COVID19-TB coinfection and discuss SARS-CoV-2 host cellular receptors and pathogenesis. In addition, we discuss M. tuberculosis host cellular receptors and pathogenesis. Moreover, we highlight the impact of SARS-CoV-2 on TB patients and the pathological pathways that connect SARS-CoV-2 and M. tuberculosis infection. Further, we discuss the impact of BCG vaccination on SARS-CoV-2 cases coinfected with M. tuberculosis, as well as the diagnostic challenges associated with the coinfection.

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G protein-coupled receptor160 regulates mycobacteria entry into macrophages by activating ERK

Cited by 8 publications

References 32 publications

Innate immunity in tuberculosis: host defense vs pathogen evasion

Innate immunity in tuberculosis: host defense vs pathogen evasion

Sphingosine-1-phosphate receptors 2 and 3 reprogram resting human macrophages into M1 phenotype following mycobacteria infection

Pathogenesis of SARS-CoV-2 and Mycobacterium tuberculosis Coinfection

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