TH-1 and TH-2 Cytokines in Stable Chronic Alcoholics

González‐Reimers, Emilio; Santolaria-Fernández, F.; Medina-García, José-A.; González-Pérez, J.M.; Vega-Prieto, Marı́a José de la; Medina-Vega, L.; Martín-González, Candelaria; Durán-Castellón, M.C.

doi:10.1093/alcalc/ags041

Cited by 22 publications

(13 citation statements)

References 43 publications

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“…In LPS-activated KCs, cytokine genes such as TNF-α, IL-1, IL-6, IL-8, IL-10, IL-12 along with IFNs, monocyte chemotactic protein (MCP)-1, platelet-derived growth factor (PDGF) and transforming growth factor β (TGF-β) are being induced. These cytokines contribute to the activation, migration and multiplication of hepatic stellate cells, increasing hepatic fibrosis and compromising liver function, but are also released into the bloodstream and might contribute to systemic symptoms such as fever, anorexia, and weight loss [11,20,21]. Patients with alcoholic hepatitis have higher circulating TNF-α levels compared to heavy drinkers with inactive cirrhosis, heavy drinkers without liver disease, and persons with neither alcoholism nor liver disease, and high levels correlate with mortality [22].…”

Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

“…Patients with alcoholic hepatitis have higher circulating TNF-α levels compared to heavy drinkers with inactive cirrhosis, heavy drinkers without liver disease, and persons with neither alcoholism nor liver disease, and high levels correlate with mortality [22]. A large number of animal and human studies have found the serum concentrations of TNF-α, IL-1, IL-6, IL-8, IL-10, IL-12, IFNs, MCP-1, PDGF, and TGF-β to be elevated in both chronic and acute alcohol-induced liver disease [11,20,21,22,23,24,25,26,27,28,29,30,31,32] (fig. 1).…”

Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

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Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Farkas

Kemény

2013

Skin Pharmacol Physiol

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Emerging evidence suggests that excessive alcohol consumption is associated with psoriasis. In alcoholics, antipsoriatic treatments are less efficient, but more toxic and an additional challenge is poor therapeutic compliance. There is a correlation between excess alcohol intake and increased risk of infections, but on the other hand alcohol and its metabolites can trigger a persistent systemic inflammation, mediated by pro-inflammatory cytokines released from activated Kupffer cells in the liver and from monocytes in the circulation. Ethanol and its metabolites can also enhance lymphocyte and keratinocyte activation and proliferation and can increase the mRNA levels of genes characteristic for proliferating keratinocytes. In this review, we discuss the mechanisms by which alcohol contributes to psoriasis development focusing on liver, systemic inflammation and skin.

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Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

Section: Alcohol Liver and Persistent Systemic Inflammationmentioning

confidence: 99%

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Farkas

Kemény

2013

Skin Pharmacol Physiol

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“…Further, chronic ethanol feeding sensitizes Kupffer cells to activation by lipopolysaccharides (LPS), leading to increased production of reactive oxygen species (ROS) and TNF-α (Park et al 2006a). Notably, chronic alcoholics have increased IL-13 and IL-10 levels but a decreased IL-4 level (González-Reimers et al 2012). IL-10 mediates antiinflammatory activity via the induction of IL-10-inducible genes, including heme oxygenase-1 (HO-1), which is an important downstream mediator of the anti-inflammatory effects of IL-10 in macrophages (O'Shea and Murray 2008).…”

Section: Discussionmentioning

confidence: 99%

Association between circulating inflammatory molecules and alcoholic liver disease in men

Jia³

et al. 2016

Cell Stress and Chaperones

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The association between alcoholic liver disease (ALD) and the inflammatory response remains controversial. The aim of this study was to explore this association between ALD and inflammation. We enrolled 214 male participants, who were divided into three age-matched groups: ALD (n = 135), chronic alcohol ingestion without ALD (non-ALD; n = 42), and control (n = 37). The BMI was significantly higher in the ALD group than in the non-ALD and control groups (all P = 0.000). Further, the constituent ratio of the liver inflammatory level was significantly higher in the ALD group than in the non-ALD and control groups (P = 0.002 and P = 0.000, respectively). In addition, the median serum ALT, AST, and GGT levels were significantly higher in the ALD group than in the control group (P = 0.023, P = 0.008, and P = 0.000, respectively); these levels were also significantly higher in the ALD group than in the non-ALD group (P = 0.013, P = 0.010, and P = 0.000, respectively). The median serum CRP level was significantly higher in the ALD group than in the non-ALD and control groups (P = 0.006 and P = 0.000, respectively). Further, the median serum TNF-α level was significantly lower in the ALD group than in the non-ALD and control groups (P = 0.004 and P = 0.000, respectively). The median serum sOX40L and HSP70 levels were significantly lower in the ALD group than in the control group (P = 0.008 and P = 0.018, respectively). In addition, the ALT, AST, and GGT levels were positively correlated with the CRP level (r = 0.211, P = 0.002; r = 0.220, P = 0.001 and r = 0.295, P = 0.000, respectively), and the GGT level was negatively correlated with the TNF-α (r = −0.225, P = 0.001), sOX40L (r = −0.165, P = 0.016), and HSP70 levels (r = −0.178, P = 0.009). Further, the Cr level was negatively correlated with the IL-10 level (r = −0.166, P = 0.015). Logistic regression analysis verified that the BMI (OR = 1.637, 95%CI: 1.374-1.951, P = 0.000) and GGT level were significantly higher (OR = 1.039, 95%CI: 1.020-1.059, P = 0.000) and that the TNF-α (OR = 0.998, 95%CI: 0.996-1.000, P = 0.030) and HSP70 levels were significantly lower (OR = 1.017, 95%CI: 1.003-1.031, P = 0.029) in the ALD group than in the non-ALD group. Further, the moderate-to-severe ALD patients had a significantly higher serum CRP level (Or = 1.349, 95%CI: 1.066-1.702, P = 0.013) and significantly lower HSP60 (OR = 0.965, 95%CI: 0.938-0.993, P = 0.014) and HSP70 levels (OR = 0.978, 95%CI: 0.962-0.995, P = 0.010) than the mild ALD patients. These results suggest that ALD patients may present with obesity, liver damage, and an imbalanced inflammatory immune response, mainly manifesting as decreased levels of immune inflammatory cytokines. In addition, they suggest that certain liver and kidney function parameters and ALD severity are either positively or negatively correlated with certain inflammatory cytokines. Hence, ALD patients may be at increased risks of obesity-and inflammation-related diseases. Accordingly, to control the inflammatory response, preventativ...

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“…In LPS-aktivierten KCs kommt es zur Induktion von Zytokingenen wie TNF-α, IL-1, IL-6, IL-8, IL-10, IL-12 sowie von IFNs, MCP-1 (Monocyte Chemotactic Protein 1), PDGF (plateletderived growth factor) und TGF-β (transforming growth factor). Diese Zytokine sind an der Aktivierung, Migration und Vermehrung hepatischer Sternzellen sowie der zunehmenden Leberfibrose und Einschränkung der Leberfunktion beteiligt; sie werden jedoch auch ins Blut abgegeben und können systemische Symptome wie Fieber, Appetitlosigkeit und Gewichtsverlust bewirken [11,20,21]. Patienten mit alkoholischer Hepatitis zeigen höhere zirkulierende TNF-α-Konzentrationen als starke Trinker mit inaktiver Zirrhose, starke Trinker ohne Lebererkrankung und Personen ohne Alkoholismus oder Lebererkrankung; zwischen erhöhten der TNF-α-Konzentration und der Mortalität besteht eine Korrelation [22].…”

Section: Alkohol Leber Und Chronische Systemische Entzündungunclassified

“…Patienten mit alkoholischer Hepatitis zeigen höhere zirkulierende TNF-α-Konzentrationen als starke Trinker mit inaktiver Zirrhose, starke Trinker ohne Lebererkrankung und Personen ohne Alkoholismus oder Lebererkrankung; zwischen erhöhten der TNF-α-Konzentration und der Mortalität besteht eine Korrelation [22]. Eine große Zahl an Tier-und Humanstudien zeigte erhöhte Serumkonzentrationen von TNF-α, IL-1, IL-6, IL-8, IL-10, IL-12, IFNs, MCP-1, PDGF und TGF-β sowohl bei chronischen als auch bei akuten alkoholinduzierten Lebererkrankungen [11,[20][21][22][23][24][25][26][27][28][29][30][31][32] (Abb. 1).…”

Section: Alkohol Leber Und Chronische Systemische Entzündungunclassified

Alkohol, Leber, systemische Entzündung und Haut: Psoriasispatienten im Fokus

Farkas¹,

Kemény²

2014

Kompass Dermatol

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Die Hinweise mehren sich, dass übermäßiger Alkoholkonsum mit Psoriasis assoziiert ist. Bei Alkoholikern sind antipsoriatische Therapien weniger wirksam, jedoch stärker toxisch und die geringe Therapie-Compliance stellt eine zusätzliche Herausforderung dar. Zwischen übermäßiger Alkoholaufnahme und einem erhöhten Infektionsrisiko besteht eine Korrelation, doch können Alkohol und seine Metaboliten andererseits eine chronische systemische Entzündung auslösen, die durch proinflammatorische Zytokine aus aktivierten Kupffer-Zellen in der Leber und Monozyten im Blutkreislauf vermittelt wird. Ethanol und seine Metaboliten können außerdem die Aktivierung und Proliferation von Lymphozyten und Keratinozyten fördern und die mRNA-Konzentration von Genen, die für proliferierende Keratinozyten charakteristisch sind, erhöhen. In dieser Übersichtsarbeit werden die Mechanismen erörtert, über die Alkohol an der Entwicklung der Psoriasis beteiligt ist, wobei der Schwerpunkt auf Leber, systemischer Entzündung und Haut liegt.

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TH-1 and TH-2 Cytokines in Stable Chronic Alcoholics

Cited by 22 publications

References 43 publications

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Alcohol, Liver, Systemic Inflammation and Skin: A Focus on Patients with Psoriasis

Association between circulating inflammatory molecules and alcoholic liver disease in men

Alkohol, Leber, systemische Entzündung und Haut: Psoriasispatienten im Fokus

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