Oxidative induction of pro-inflammatory cytokine formation by human monocyte-derived macrophages following exposure to manganese<i>in vitro</i>

Mokgobu, Matlou Ingrid; Cholo, Moloko C.; Anderson, Ronald; Steel, Helen C.; Motheo, Maraki P; Hlatshwayo, Thembani N; Tintinger, Gregory Ronald; Theron, Annette J.

doi:10.3109/1547691x.2014.902877

Cited by 21 publications

(20 citation statements)

References 24 publications

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“…Cytokines have been increasingly implicated in acute and chronic neuronal degeneration [45]. Recent clinical studies have reported increased levels of TNF-, IL-6, IL-1b, and interferon- in post-mortem brain tissues [46,47]. In our study, we observed strong relationships between the levels of Mn and of the pro-infl ammatory cytokines IL-6 and TNF-, as well as the adhesion marker sE-selectin.…”

Section: Discussionsupporting

confidence: 66%

Pro-inflammatory cytokine and vascular adhesion molecule levels in manganese and lead-exposed workers

Öztan¹,

Türksoy²,

Daltaban³

et al. 2019

Int J Immunother Cancer Res

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Constitutive neurogenesis affects both children and adults and is known to correlate closely with neurocognitive functions such as learning and memory [1]. Infl ammation is a systemic reaction. However, the brain reacts to infl ammation differently than peripheral tissues. Under normal conditions, the Blood-Brain Barrier (BBB) is selectively permeable and allows only the passage of T-cells, macrophages, and dendritic cells [2]. However, infl ammation of the brain initiates the secretion of anti-and pro-infl ammatory cytokines by resident microglia, astrocytes, infi ltrating peripheral macrophages, and lymphocytes. This activity both stimulates the migration of leukocytes to the region and promotes astrogliosis [3]. Pathologically, Parkinson's Disease (PD) is characterized by the massive degeneration and loss of nigrostriatal dopaminergic neurons. Many studies of PD have also emphasized the

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Section: Discussionsupporting

confidence: 66%

Pro-inflammatory cytokine and vascular adhesion molecule levels in manganese and lead-exposed workers

Öztan¹,

Türksoy²,

Daltaban³

et al. 2019

Int J Immunother Cancer Res

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“…To determine if the decrease in M1 polarization as measured by cell surface and gene expression changes its function, we used carboxy‐H2CDFDA to detect ROS production via flow cytometry as macrophages produce ROS in order to neutralize pathogens (Mokgobu et al ., ). Stimulating macrophages towards an M1 phenotype with LPS + IFN‐γ demonstrated a greater capacity to produce ROS compared with basal levels observed in M0 macrophages.…”

Section: Resultsmentioning

confidence: 97%

“…Asides from examining M1 phenotype using cell surface markers and gene expression of M1‐associated cytokines, the effect of HDL on the functional capacity of LPS + IFN‐γ‐induced M1 macrophages was examined. Our data confirms an increase in ROS generation in M1 macrophages (Mokgobu et al ., ) where it is likely to trigger activation of the NFκB pathway, and in turn increase inflammatory cytokines expression (Fenyo and Gafencu, ). Furthermore, in the setting of atherosclerosis, oxidative modification of LDLs induced by ROS results in an increase in foam cell formation (Yla‐Herttuala, ).…”

Section: Discussionmentioning

confidence: 99%

High‐density lipoprotein inhibits human M1 macrophage polarization through redistribution of caveolin‐1

Lee

Moore

et al. 2015

British J Pharmacology

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BACKGROUND AND PURPOSEMonocyte-derived macrophages are critical in the development of atherosclerosis and can adopt a wide range of functional phenotypes depending on their surrounding milieu. High-density lipoproteins (HDLs) have many cardio-protective properties including potent anti-inflammatory effects. We investigated the effects of HDL on human macrophage phenotype and the mechanisms by which these occur. EXPERIMENTAL APPROACHHuman blood monocytes were differentiated into macrophages in the presence or absence of HDL and were then induced to either an inflammatory macrophage (M1) or anti-inflammatory macrophage (M2) phenotype using LPS and IFN-γ or IL-4, respectively. KEY RESULTSHDL inhibited the induction of macrophages to an M1-phenotype, as evidenced by a decrease in the expression of M1-specific cell surface markers CD192 and CD64, as well as M1-associated inflammatory genes TNF-α, IL-6 and MCP-1 (CCL2). HDL also inhibited M1 function by reducing the production of ROS. In contrast, HDL had no effect on macrophage induction to the M2-phenotype. Similarly, methyl-β-cyclodextrin, a non-specific cholesterol acceptor also suppressed the induction of M1 suggesting that cholesterol efflux is important in this process. Furthermore, HDL decreased membrane caveolin-1 in M1 macrophages. We confirmed that caveolin-1 is required for HDL to inhibit M1 induction as bone marrow-derived macrophages from caveolin-1 knockout mice continued to polarize into M1-phenotype despite the presence of HDL. Moreover, HDL decreased ERK1/2 and STAT3 phosphorylation in M1 macrophages. CONCLUSIONS AND IMPLICATIONSWe concluded that HDL reduces the induction of macrophages to the inflammatory M1-phenotype via redistribution of caveolin-1, preventing the activation of ERK1/2 and STAT3. LINKED ARTICLES

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“…ROS could also directly induce inflammatory cytokine expression/production via regulation of immune signaling through TLR4-mediated NF-κB activation [28]. It was reported that the Mn 2+ -mediated induction of inflammatory cytokine production was associated with increased production of H 2 O 2 , and effectively attenuated by the H 2 O 2 - scavenger dithiothreitol, and partially prevented by inhibitors of NF-κB and p38MAP kinase [43]. ROS has been shown to induce gene expression of inflammatory mediators, such as IL-1 and TNF-a [44].…”

Section: Discussionmentioning

confidence: 99%

Ambient Fine Particulate Matter Induces Apoptosis of Endothelial Progenitor Cells Through Reactive Oxygen Species Formation

Cui¹,

Xie²,

Jia³

et al. 2015

Cell Physiol Biochem

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Background/Aims: Bone marrow (BM)-derived endothelial progenitor cells (EPCs) play a critical role in angiogenesis and vascular repair. Some environmental insults, like fine particulate matter (PM) exposure, significantly impair cardiovascular functions. However, the mechanisms for PM-induced adverse effects on cardiovascular system remain largely unknown. The present research was to study the detrimental effects of PM on EPCs and explore the potential mechanisms. Methods: PM was intranasal-distilled into male C57BL/6 mice for one month. Flow cytometry was used to measure the number of EPCs, apoptosis level of circulating EPCs and intracellular reactive oxygen species (ROS) formation. Serum TNF- α and IL-1β were measured using ELISA. To determine the role of PM-induced ROS in EPC apoptosis, PM was co-administrated with the antioxidant N-acetylcysteine (NAC) in wild type mice or used in a triple transgenic mouse line (TG) with overexpression of antioxidant enzyme network (AON) composed of superoxide dismutase (SOD)1, SOD3, and glutathione peroxidase (Gpx-1) with decreased in vivo ROS production. Results: PM treatment significantly decreased circulating EPC population, promoted apoptosis of EPCs in association with increased ROS production and serum TNF-α and IL-1β levels, which could be effectively reversed by either NAC treatment or overexpression of AON. Conclusion: PM exposure significantly decreased circulating EPCs population due to increased apoptosis via ROS formation in mice.

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Oxidative induction of pro-inflammatory cytokine formation by human monocyte-derived macrophages following exposure to manganesein vitro

Cited by 21 publications

References 24 publications

Pro-inflammatory cytokine and vascular adhesion molecule levels in manganese and lead-exposed workers

Pro-inflammatory cytokine and vascular adhesion molecule levels in manganese and lead-exposed workers

High‐density lipoprotein inhibits human M1 macrophage polarization through redistribution of caveolin‐1

Ambient Fine Particulate Matter Induces Apoptosis of Endothelial Progenitor Cells Through Reactive Oxygen Species Formation

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