TNFR/TNF-α signaling pathway regulates apoptosis of alveolar macrophages in coal workers' pneumoconiosis

Qin, Qian; Cao, Xiaohong; Liu, Haiyan; Zheng, Gen; Qian, Qingqiang; Shen, Fuhai

doi:10.18632/oncotarget.18921

Cited by 8 publications

(8 citation statements)

References 38 publications

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“…We found that none of RipK3, Irf3 or Irf7 contributed to the down-regulation of IFNGR1 in LPS treated macrophages. 15,38,39 The lack of a role for Irf3 and Irf7 supports our finding that type I IFNs do not play a role in IFNGR1…”

Section: Discussionsupporting

confidence: 81%

“…Myd88‐ and Trif‐mediated signaling cascades induce NF‐κB activation, leading to the expression of numerous pro‐inflammatory cytokines . To investigate whether NF‐κB activation contributed to down‐regulation of IFNGR1 in LPS treated macrophages, NF‐κB activation was inhibited in iBMDM using the NF‐κB inhibitor BAY 11–7085, which irreversibly inhibits IκBα phosphorylation and prevents its degradation, thereby preventing NF‐κB translocation into the nucleus .…”

Section: Resultsmentioning

confidence: 99%

“…Irf3 and Irf7 are highly homologous and are the key transcription factors responsible the induction of type I IFNs . NF‐κB is a crucial and central regulator of gene expression for cell survival, cell death, inflammation, and immune response . Inhibition of NF‐κB activation using BAY 11–7085 also significantly reduced down‐regulation of IFNGR1 in macrophages upon treatment with LPS or heat‐killed L. pneumophila , suggesting that MyD88‐ and/or Trif‐mediated NF‐κB activation was required for the reduction in IFNGR1 expression in infected or stimulated macrophages.…”

Section: Discussionmentioning

confidence: 99%

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IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages

Yang

McDermot

Pasricha

et al. 2019

Journal of Leukocyte Biology

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Legionella pneumophila is an opportunistic human pathogen and causative agent of the acute pneumonia known as Legionnaire's disease. Upon inhalation, the bacteria replicate in alveolar macrophages (AM), within an intracellular vacuole termed the Legionella-containing vacuole. We recently found that, in vivo, IFN was required for optimal clearance of intracellular L. pneumophila by monocyte-derived cells (MC), but the cytokine did not appear to influence clearance by AM. Here, we report that during L. pneumophila lung infection, expression of the IFN receptor subunit 1 (IFNGR1) is down-regulated in AM and neutrophils, but not MC, offering a possible explanation for why AM are unable to effectively restrict L. pneumophila replication in vivo. To test this, we used mice that constitutively express IFNGR1 in AM and found that prevention of IFNGR1 down-regulation enhanced the ability of AM to restrict L. pneumophila intracellular replication. IFNGR1 down-regulation was independent of the type IV Dot/Icm secretion system of L. pneumophila indicating that bacterial effector proteins were not involved. In contrast to previous work, we found that signaling via type I IFN receptors was not required for IFNGR1 down-regulation in macrophages but rather that MyD88-or Trif-mediated NF-B activation was required. This work has uncovered an alternative signaling pathway responsible for IFNGR1 down-regulation in macrophages during bacterial infection.

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Section: Discussionsupporting

confidence: 81%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages

Yang

McDermot

Pasricha

et al. 2019

Journal of Leukocyte Biology

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“…CWP is a serious occupational disease in China [ 24 ]. A steady decrease in the number of coal miners exposed to dust in developed countries has played a crucial role.…”

Section: Discussionmentioning

confidence: 99%

Time trends and future prediction of coal worker’s pneumoconiosis in opencast coal mine in China based on the APC model

Xian

et al. 2018

BMC Public Health

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BackgroundThe opencast coal mine is a specific mine differing from the underground mine. There are differences in the way into the ore body, the organization of production, transport technology and other aspects. This study aimed to describe the prevalence of CWP among ex-dust miners in opencast coal mines and estimate the incidence trend of CWP by APC model in the future.MethodsAll opencast miners who had been exposed to dust for at least 1 year in opencast mines were enrolled in this study. The database included demographic details, occupational history records with the date of dust exposure, physical examination records and pneumoconiosis diagnosis records. An age-period-cohort (APC) model has been carried out in order to explore the effects of the age, period and cohort on the prevalence of CWP among ex-dust opencast miners.Results8191 opencast miners were enrolled in the study, including 259 miners with CWP and 7932 miners without CWP. The incidence density of CWP would have an increasing trend in opencast mines from 2005 to 2024. The number of possible CWP patients predicted in this period was approximately 492. Of them, 275 miners could have suffered from CWP in 2005–2014 and 217 miners would suffer from CWP in 2015–2024 among the ex-dust opencast miners.ConclusionsThe APC model had a goodness of fit in predicting the incidence trend of CWP in opencast coal mines. By this model, we predicted that 492 opencast miners could be diagnosed as CWP from 2005 to 2024. Therefore ex-dust opencast miners cannot be ignored and they should have regular physical examinations and detection for CWP.Electronic supplementary materialThe online version of this article (10.1186/s12889-018-5937-0) contains supplementary material, which is available to authorized users.

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“…In particular, TNF-a has significant effects [9][10][11][12] . TNF-a induces apoptosis of tumor cells by combining with the TNF receptor (TNFR) 13,14 on the cytomembrane. It can also promote the proliferation and differentiation of immune cells and impose antitumor effects.…”

Section: Introductionmentioning

confidence: 99%

Effects of Rapamycin Combined with Cisplatin on Tumor Necrosis Factor TNF-α in MG-63 Cells

Han

et al. 2020

Cell Transplant

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Rapamycin (RAPA) and cisplatin (CDDP) are used as clinical drugs in the treatment of various tumors, but there are few studies on the combination of RAPA and CDDP. Tumor necrosis factor α (TNF-α) plays an important role in tumorigenesis and development. This study is to explore the effects of RAPA combined with CDDP on the expression of TNF-α in osteosarcoma MG-63 cells. MG-63 cells were routinely cultured and divided into a control group, a RAPA group (20 μM), a CDDP group (20 μM), and a RAPA + CDDP group (20 μM + 20 μM). The four groups were treated with drugs for 24 and 48 h, respectively. Real-time polymerase chain reaction (PCR), Western blot (WB), and immunocytochemistry (ICC) were adopted to detect the expression of TNF-α gene and protein. The results of PCR showed that both the separate drug use and drug combination could significantly lower the relative expression quantity of TNF-α gene (* P < 0.5), but the combination was more effective (* P < 0.5); the expression quantity of TNF-α gene in the RAPA + CDDP group at 48 h was much lower than that at 24 h (*** P < 0.001). The results of WB showed that both the separate drug use and drug combination could significantly lower the relative expression quantity of TNF-α protein, and the combination was more effective than separate drug use (* P < 0.05) and more effective at 48 h (*** P < 0.001); the expression quantity of TNF-α protein in the same group at 48 h was much lower than that at 24 h (* P < 0.05). The results of ICC showed that both the separate drug use and drug combination could significantly lower the relative expression quantity of TNF-α protein, and the combination was more effective than separate drug use (** P < 0.01) and more effective at 48 h (*** P < 0.001); the expression quantity of TNF-α protein in the same group at 48 h was much lower than that at 24 h (** P < 0.01). RAPA combined with CDDP can significantly reduce the expression of TNF-α in MG-63 cells, which is time dependent.

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TNFR/TNF-α signaling pathway regulates apoptosis of alveolar macrophages in coal workers' pneumoconiosis

Cited by 8 publications

References 38 publications

IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages

IFNγ receptor down-regulation facilitates Legionella survival in alveolar macrophages

Time trends and future prediction of coal worker’s pneumoconiosis in opencast coal mine in China based on the APC model

Effects of Rapamycin Combined with Cisplatin on Tumor Necrosis Factor TNF-α in MG-63 Cells

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