Effects of ethanol on cytokine generation and NFκB activity in human lung epithelial cell

Johansson, Anne-Sofie M.; Lidén, Johan; Okret, Sam; Palmblad, Jan

doi:10.1016/j.bcp.2005.05.016

Cited by 9 publications

(10 citation statements)

References 44 publications

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“…Interestingly, both IL-6 and IL-8 are modulated by alcohol: while chronic alcohol consumption has been proven to increase their expression and release, acute alcohol consumption reduced the lipopolysaccharide (LPS)-induced IL-6 release from macrophages (44). Short-term alcohol exposure reduced IL-8 release from human umbilical vein cells (HUVECs) or lung epithelial cells, but considerable inhibitory effects on the cellular interactions with neutrophils were also noted, suggesting that reduced nuclear translocation of NF-κB components was also involved (21,22). In the present study, IL-8 release from lung epithelial cells after stimulation with either IL-1β or TNF was markedly reduced by EtOH and EtP treatment (Fig.…”

Section: Discussionsupporting

confidence: 47%

“…By contrast, studies on acute and/or low-dose to moderate alcohol intake have indicated potentially beneficial anti-inflammatory effects (16)(17)(18)(19)(20). Johansson et al and others have reported on the alcohol-reduced release of interleukin-8 (IL-8) in human endothelial and epithelial cells, their decreased interaction with neutrophils and reduced translocation of nuclear factor-κB (NF-κB) components into the nucleus (21,22). Previously, we have shown that acute alcohol consumption diminished both liver and systemic IL-6 increase, and also hepatic neutrophil infiltration in a model of acute inflammation in vivo (18).…”

Section: Introductionmentioning

confidence: 99%

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Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells

Relja

Omid

Wagner

et al. 2015

International Journal of Molecular Medicine

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Abstract. Increases in pro-inflammatory cytokine levels and tissue-infiltrating leukocytes have been closely linked to increased systemic and local inflammation, which result in organ injury. Previously, we demonstrated the beneficial and hepatoprotective anti-inflammatory effects of acute ethanol (EtOH) ingestion in an in vivo model of acute inflammation. Due to its undesirable side-effects, however, EtOH does not represent a therapeutic option for treatment of acute inflammation. Therefore, in this study, we compared the effects of acute EtOH exposure with ethyl pyruvate (EtP) as an alternative anti-inflammatory drug in an in vitro model of hepatic and pulmonary inflammation. Human hepatocellular carcinoma cells Huh7 and alveolar epithelial cells A549 were stimulated with either interleukin (IL) IL-1β (1 ng/ml, 24 h) or tumor necrosis factor (TNF) (10 ng/ml, 4 h), and then treated with EtP (2.5-10 mM), sodium pyruvate (NaP, 10 mM) or EtOH (85-170 mM) for 1 h. IL-6 or IL-8 release from Huh7 or A549 cells, respectively, was measured by an enzyme-linked immunosorbent assay. Neutrophil adhesion to cell monolayers and CD54 expression were also analyzed. Bcl-2 and Bax gene expression was determined by RT-qPCR, and western blot analysis was performed to determine the mechanisms involved. Treating A549 cells with either EtOH or EtP significantly reduced the IL-1β-or TNF-induced IL-8 release, whereas treating Huh7 cells did not significantly alter IL-6 release. Similarly, neutrophil adhesion to stimulated A549 cells was significantly reduced by EtOH or EtP, whereas for Huh7 cells the tendency for reduced neutrophil adhesion rates by EtOH or EtP was not significant. CD54 expression was noticeably reduced in A549 cells, but this was not the case in Huh7 cells after treatment. The Bax/ Bcl-2 ratio was dose-dependently decreased by EtOH and by high-dose EtP in A549 cells, indicating a reduction in apoptosis, whereas this effect was not observed in Huh7 cells. The underlying mechanisms involve reduced phosphorylation of Akt and nuclear factor-κB (NF-κB) p65. We noted that as with EtP, EtOH reduced the inflammatory response in lung epithelial cells under acute inflammatory conditions. However, due to the low impact which EtP and EtOH had on the hepatocellular cells, our data suggest that both substances exerted different effects depending on the cellular entity. The possible underlying mechanisms involved the downregulation of Akt and the transcription factor NF-κB, but further research on this subject is required.

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Section: Discussionsupporting

confidence: 47%

Section: Introductionmentioning

confidence: 99%

Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells

Relja

Omid

Wagner

et al. 2015

International Journal of Molecular Medicine

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“…We have previously reported that stimulated A549 cells produce large amounts of several cytokines, including IL-8, G-CSF and GM-CSF (Johansson et al 2005). EtP was reported to reduce the production of these cytokines by about 50% in stimulated HUVECs (Johansson et al 2008).…”

Section: Cytokine Releasementioning

confidence: 98%

“…The human lung adenocarcinoma cell line A549 was a kind gift from Dr. Magnus Nord at Karolinska Institutet and was cultured as previously described (Johansson et al 2005).…”

Section: Cell Cultures and Viabilitymentioning

confidence: 99%

Ethyl pyruvate modulates adhesive and secretory reactions in human lung epithelial cells

Johansson

Palmblad

2009

Life Sciences

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“…Commonly, M-CSF secreted by cells, binds to its transmembrane receptor which leads to the transduction of the signal onto the target cell; then the M-CSF-receptor complex is internalized after accomplishing its function and degraded; therefore, M-CSF is usually not found in the cells. However, recent studies have shown that M-CSF can be expressed at a high level in the cytoplasm and nuclei of some kinds of malignant tumors [23][24][25]. The process is associated with enhanced tumor cells' movement and invasion, resulting in an unfavorable prognosis, which suggests that intracellular expression of M-CSF may have some specific action.…”

Section: Discussionmentioning

confidence: 99%

Nuclear M-CSF Accelerates DNA Replication and Cell Proliferation in HeLa Human Cervical Cancer Cells

Tu¹

2017

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Macrophage colony-stimulating factor (M-CSF), also named colony-stimulating factor-1 (CSF-1), plays an important role in the process of proliferation and differentiation of the monocyte/macrophage lineage cells. Commonly, it is not easy to measure the expression of cellular M-CSF. However, recent studies have shown that M-CSF can be expressed at a high level in the cytoplasm and nuclei of some kinds of malignant tumors, which related to the poor prognosis. To explore the role and mechanism of nuclear M-CSF, in the present study we constructed the pCMV/nuc/M-CSF vector and transfected it into human HeLa nuclei. The results from our previous study indicated, M-CSF was stably expressed in HeLa nuclei, which were used as a model to determine the nuclear effects of M-CSF. There was a higher percentage of replicating nuclei in the transfected pCMV/nuc/M-CSF HeLa cells both in phase G1 and S. According to the data from the cell doubling time, antisense oligonucleotides and the experiments of the transplanted tumor in nude mice, nuclear M-CSF could promote the cell proliferation of HeLa cells both in vivo and in vitro. In conclusion, nuclear M-CSF could accelerate DNA replication and cell proliferation of cervical carcinoma.

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Effects of ethanol on cytokine generation and NFκB activity in human lung epithelial cell

Cited by 9 publications

References 44 publications

Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells

Ethanol, ethyl and sodium pyruvate decrease the inflammatory responses of human lung epithelial cells via Akt and NF-κB in vitro but have a low impact on hepatocellular cells

Ethyl pyruvate modulates adhesive and secretory reactions in human lung epithelial cells

Nuclear M-CSF Accelerates DNA Replication and Cell Proliferation in HeLa Human Cervical Cancer Cells

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