Kupffer cells and alcoholic liver disease

Cubero, Francisco Javier; Nieto, Natalia

doi:10.4321/s1130-01082006000600007

Cited by 30 publications

(25 citation statements)

References 111 publications

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“…It is generally believed that elevated hepatic LPS in response to alcohol consumption stimulates Kupffer cells to produce various factors that activate hepatic stellate cells (HSCs). In addition, LPS also directly targets HSCs and enhances pro‐fibrogenic cytokine transforming growth factor β (TGF‐β) signaling on these cells, subsequently leading to HSC activation and liver fibrosis (Cubero and Nieto, 2006; Cubero et al., 2009; Guo et al., 2009; Seki et al., 2007). Furthermore, ethanol and its metabolite acetaldehyde can directly induce HSC activation (Cubero et al., 2009).…”

Section: Anti‐fibrotic Effect Of Nk Cells/ifn‐γ: Suppression By Alcoholmentioning

confidence: 99%

Molecular Mechanisms of Alcoholic Liver Disease: Innate Immunity and Cytokines

Miller

Horiguchi²,

Jeong³

et al. 2011

Alcoholism: Clinical and Experimental Research

152

133

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Alcohol consumption is a predominant etiological factor in the pathogenesis of chronic liver diseases worldwide, causing fatty liver, alcoholic hepatitis, fibrosis/cirrhosis, and hepatocellular carcinoma. In the past few decades, significant progress has been made in our understanding of the molecular mechanisms underlying alcoholic liver injury. Activation of innate immunity components such as Kupffer cells, LPS/TLR4, and complements in response to alcohol exposure plays a key role in the development and progression of alcoholic liver disease (ALD). LPS activation of Kupffer cells also produces IL-6 and IL-10 that may play a protective role in ameliorating ALD. IL-6 activates signal transducer and activator of transcription 3 (STAT3) in hepatocytes and sinusoidal endothelial cells, while IL-10 activates STAT3 in Kupffer cells/macrophages, subsequently protecting against ALD. In addition, alcohol consumption also inhibits some components of innate immunity such as natural killer (NK) cells, a type of cells that play key roles in anti-viral, anti-tumor, and anti-fibrotic defenses in the liver. Ethanol inhibition of NK cells likely contributes significantly to the pathogenesis of ALD. Understanding the roles of innate immunity and cytokines in alcoholic liver injury may provide insight into novel therapeutic targets in the treatment of alcoholic liver disease.

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Section: Anti‐fibrotic Effect Of Nk Cells/ifn‐γ: Suppression By Alcoholmentioning

confidence: 99%

Molecular Mechanisms of Alcoholic Liver Disease: Innate Immunity and Cytokines

Miller

Horiguchi²,

Jeong³

et al. 2011

Alcoholism: Clinical and Experimental Research

152

133

View full text Add to dashboard Cite

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“…Excess of NADH promotes the synthesis and deposition of triglycerides in the liver. This leads to the development of the first stage of alcoholic liver disease, which is steatosis [46][47][48]. Then, as a result of continued chronic ethanol intake, chronic hepatitis occurs (stage 2), resulting in fibrosis of the organ and in the final stage may lead to its cirrhosis (stage 3) [49].…”

Section: Cirrhosis Of the Livermentioning

confidence: 99%

An overlooked issue: sexual dysfunctions in men addicted to alcohol

Siembida

Frończuk²,

Morylowska-Topolska

et al. 2018

Curr Probl Psychiatry

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Introduction According to the data obtained in the EZOP Poland study (2015), the prevalence of alcohol dependence in lifetime in Poland amounts to about 2.2% of the population, entailing enormous social, family and personal harm, including health damage. It is estimated that about 72% of alcohol-dependent patients complain about one or more problems related to the sexual sphere, which may result from both the development of somatic complications in the course of alcohol dependence, and from psychiatric complications that themselves can lead to sexual dysfunction. There are reports and clinical observations indicating that the occurrence of sexual dysfunction (SD) can affect the shortening or interruption of the period of abstinence. Aim The aim of this work is to show sexual dysfunctions in alcohol-dependent men and to discuss the factors that may affect the occurrence of the above-mentioned dysfunctions. Material and methods The available literature was reviewed using Medline, Google Scholar and ScienceDirect browsers by entering the keywords: alcohol dependence, sexual dysfunction, comorbidity, alcohol-caused diseases and time descriptors: 1979-2016. Results • Alcohol dependence is associated with the occurrence of various types of sexual dysfunctions (SD). • The diagnosis of SD should take into account all possible causes that may lead to the development of SD in this group of patients, including the comorbidity of somatic diseases or the negative impact of drugs on sexual function. • Occurrence of SD is connected with a higher risk of abstinence interruption. • There is a need to carry out more research in order to better understand the relationship between alcohol dependence and the prevalence of sexual dysfunctions.

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“…Los hepatocitos y las células de Kupffer son una gran fuente de ERO y de especies reactivas de nitrógeno, que estimulan de forma paracrina a las CEH (27)(28)(29)(30)(31). Además, su actividad se magnifica in vivo por la depleción de antioxidantes como ocurre en las hepatopatías (32).…”

Section: Activación De Células Estrelladas Y Fibrosis Hepáticaunclassified

“…•-se produce también durante la generación de estrés oxidativo en la fagocitosis (31). Una oxidasa de la explosión respiratoria de la membrana cataliza la reducción monoelectrónica del O 2 en O 2…”

Section: Efecto Paracrino De Las Células De Kupfferunclassified

Células estrelladas hepáticas y estrés oxidativo

Urtasun

Nieto

2007

Rev. esp. enferm. dig.

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RESUMENLa fibrosis hepática ocurre en la lesión hepática crónica y se caracteriza por la producción excesiva y el depósito de componentes de la matriz extracelular (MEC), fundamentalmente de colágeno de tipo I. Las células estralladas hepáticas (CEH) son las responsables de la producción excesiva de matriz extracelular durante la fibrosis. La activación de las CEH, constituye el paso fundamental del desarrollo de la fibrosis hepática y está mediada por citoquinas específicas y especies reactivas de oxígeno (ERO) que liberan los hepatocitos dañados, las células de Kupffer y las CEH activadas. Aunque las CEH permanecen normalmente en estado quiescente, se activan en respuesta a los factores que promueven la lesión hepática y proliferan y generan matriz. Un rasgo fundamental de la activación de las CEH es la producción incontrolada de colágeno de tipo I con una escasa degradación. El colágeno es una proteína heterotrimérica que se compone de dos cadenas α1 y una cadena α2, formando una triple hélice. El inicio de la activación de las células estrelladas se debe en gran medida a una estimulación paracrina, mientras que la perpetuación de dicho estado activado implica regulación tanto autocrina como paracrina. Esta revisión trata del papel del estrés oxidativo sobre la activación de las CEH.Palabras clave: Células estrelladas hepáticas. Fibrosis. Matriz extracelular. Especies reactivas de oxígeno. ABSTRACTHepatic fibrosis is a wound-healing response that takes place during chronic liver injury and is characterized by excessive production and deposition of extracellular matrix (ECM) components, mainly collagen type I. Hepatic stellate cells (HSC) are responsible for the excessive production of scar tissue during liver fibrosis. Activation of HSC, the main step in the development of hepatic fibrosis, is mediated by specific cytokines and reactive oxygen species (ROS) released by damaged hepatocytes and/or activated Kupffer cells and HSC. While HSC usually remain quiescent, in response to factors promoting liver injury they undergo activation and become highly proliferative and fibrogenic. Indeed a key feature of HSC activation is uncontrolled production of collagen type I with very little degradation. Collagen is a heterotrimeric protein composed of two α1 chains and one α2 chain forming a triple helix structure. Initiation of stellate cell activation is largely due to paracrine stimulation, whereas the perpetuation of such activated state involves autocrine as well as paracrine loops. This review focuses on the role of oxidant stress on the activation of stellate cells.

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Kupffer cells and alcoholic liver disease

Cited by 30 publications

References 111 publications

Molecular Mechanisms of Alcoholic Liver Disease: Innate Immunity and Cytokines

Molecular Mechanisms of Alcoholic Liver Disease: Innate Immunity and Cytokines

An overlooked issue: sexual dysfunctions in men addicted to alcohol

Células estrelladas hepáticas y estrés oxidativo

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