M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells

Cui, Jiahuan; Xu, Wan; Chen, Jian; Dai, Lu; Frank, Jacqueline A.; Peng, Shaojun; Wang, Siying; Chen, Gang

doi:10.18632/oncotarget.15232

Cited by 30 publications

(20 citation statements)

References 24 publications

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“…The M1-like microglia phenotype produces proinflammatory cytokines (TNF-alpha, IL-1beta, IL-6, IL-12 and an array of cytotoxic molecules) [46,47]. We could assume an M2-like microglia phenotype that would produce, just like macrophages, anti-inflammatory cytokines (IL-10, IL-4, TGF-beta, other neurotrophic factors, and chemokines CCL17 and CCL18) [23,42,[48][49][50]. Generally, M2 activation is more involved in the resolution of inflammation and tissue repair.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Chitotriosidase and CC-Chemokine Ligand 18 as Biomarkers of Microglia Activation in Amyotrophic Lateral Sclerosis

et al. 2018

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Background: The development of biomarkers for use in diagnosing, monitoring disease progression and analyzing therapeutic trials response in amyotrophic lateral sclerosis (ALS) is essential. Objective: The aim of this study was to identify inflammatory factors in plasma or cerebrospinal fluid (CSF) from patients with ALS with particular attention to specific markers of microglia activation as chitotriosidase (ChT) and chemokine (C-C motif) ligand 18 (CCL18) to determine its potential as ALS biomarkers. Methods: We studied CSF and plasma samples from 32 patients and 42 healthy controls. We assayed the ChT activity by a spectrofluorometric method and protein levels of other inflammatory biomarkers (tumor necrosis factor [TNF]-alpha, interleukin [IL]-6 and CCL18) by enzyme-linked immunosorbent assay. CHIT1 gene polymorphism in exon 10 (c.1049_1072dup24) encoding inactive ChT enzyme was genotyped in all subjects. Results: ChT activity and TNF-alpha protein levels were significantly higher in CSF of ALS patients, but we found no correlation with the severity and progression of the disease. Nevertheless, we did not found any differences in CCL18 or IL-6 protein levels between both groups in CSF or plasma. In our sample, only 3% of subjects were homozygous carriers for the CHIT1 exon 10 duplication associated with defective enzyme. Conclusions: High ChT activity in CSF of patients with ALS may reflect microglia activation and could be a potential biomarker of the disease. We did not find any significant difference regarding CCL-18, another specific marker of microglia activation that is related with M2-like microglia phenotype. Deepening the understanding of the activation state of microglia (M1 and M2) may contribute to the knowledge about the specific role of neuroinflammation in ALS and future therapeutic strategies.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Chitotriosidase and CC-Chemokine Ligand 18 as Biomarkers of Microglia Activation in Amyotrophic Lateral Sclerosis

et al. 2018

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“…Recently, macrophage polarization has been found out to play very critical roles in numerous diseases, e.g. tumor formation [ 18 – 21 ], tissue repair [ 22 – 24 ], and cell proliferation [ 20 , 25 – 29 ]. Compared to adoptive transfer of M2 macrophages, in vivo polarization of macrophages may be a more powerful and clinic-applicable method, since macrophage polarization in vivo not only increases M2 macrophages, but also reduces M1 macrophages, resulting in two beneficial effects of further increases in production of trophic growth factors and removal of the detrimental effects from M1 macrophages [ 25 , 30 – 32 ].…”

Section: Discussionmentioning

confidence: 99%

Interleukin-13 reduces cardiac injury and prevents heart dysfunction in viral myocarditis via enhanced M2 macrophage polarization

2017

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Viral myocarditis is one of the major causes of congestive heart failure and dilated cardiomyopathy. Recent reports have demonstrated an essential role of cytokines, like interleukin-13 (IL-13), in the pathogenesis of viral myocarditis, while the underlying mechanisms remain poorly defined. Here, using a coxsackie virus B3 (CVB3)-infection model in BALB/C mice, we showed that IL-13 protected mouse heart function in viral myocarditis, seemingly through reduction in T lymphocyte immunity and induction of M2 macrophage polarization. Adoptive transfer to M2 macrophages mimicked the effects of IL-13 on protection from myocarditis, suggesting that the effects of IL-13 may be primarily through regulation of macrophage polarization. Together, our data suggest that application of IL-13 treatment may reduce cardiac Injury and protect heart function in viral myocarditis via enhanced M2 macrophage polarization.

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“…Arsenic exposure was shown to reduce surface markers of macrophages while enhancing monocytic markers in circulating monocytes, resulting in rapid cell rounding and subsequent loss of adhesion 52 . Arsenic treatment was found to alter polarization of macrophages to M2 status, in which macrophages show increased IL-10 and TGF-β levels 53 . Thus, arsenic exposure blocks inflammatory responses of macrophages, which recognize and eliminate harmful signals such as endogenous and exogenous antigens through inhibition of pro-inflammatory cytokines.…”

Section: Discussionmentioning

confidence: 99%

Mercury and arsenic attenuate canonical and non-canonical NLRP3 inflammasome activation

Ahn

Kim

Kang

et al. 2018

Sci Rep

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Exposure to heavy metals can cause several diseases associated with the immune system. Although the effects of heavy metals on production of inflammatory cytokines have been previously studied, the role of heavy metals in inflammasome activation remains poorly studied. The inflammasome is an intracellular multi-protein complex that detects intracellular danger signals, resulting in inflammatory responses such as cytokine maturation and pyroptosis. In this study, we elucidated the effects of four heavy metals, including cadmium (Cd), mercury (Hg), arsenic (As), and lead (Pb), on the activation of NLRP3, NLRC4, and AIM2 inflammasomes. In our results, mercury and arsenic inhibited interleukin (IL)-1β and IL-18 secretion resulting from canonical and non-canonical NLRP3 inflammasome activation in macrophages and attenuated elevation of serum IL-1β in response to LPS treatment in mice. In the mechanical studies, mercury interrupted production of mitochondrial reactive oxygen species, release of mitochondrial DNA, and activity of recombinant caspase-1, whereas arsenic down-regulated expression of promyelocytic leukemia protein. Both mercury and arsenic inhibited Asc pyroptosome formation and gasdermin D cleavage. Thus, we suggest that exposure to mercury and/or arsenic could disrupt inflammasome-mediated inflammatory responses, which might cause unexpected side effects.

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M2 polarization of macrophages facilitates arsenic-induced cell transformation of lung epithelial cells

Cited by 30 publications

References 24 publications

Evaluation of Chitotriosidase and CC-Chemokine Ligand 18 as Biomarkers of Microglia Activation in Amyotrophic Lateral Sclerosis

Evaluation of Chitotriosidase and CC-Chemokine Ligand 18 as Biomarkers of Microglia Activation in Amyotrophic Lateral Sclerosis

Interleukin-13 reduces cardiac injury and prevents heart dysfunction in viral myocarditis via enhanced M2 macrophage polarization

Mercury and arsenic attenuate canonical and non-canonical NLRP3 inflammasome activation

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