Meeting reportEthanol and cytokine secretion
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Dimerumic acid and deferricoprogen produced by Monascus purpureus attenuate liquid ethanol diet-induced alcoholic hepatitis via suppressing NF-κB inflammation signalling pathways and stimulation of AMPK-mediated lipid metabolism
2019, Journal of Functional FoodsCitation Excerpt :The results didn’t observe lipid accumulation in the liver tissue in the SL, DMA-H and DFC-H groups. Alcohol abuse results in liver injury because macrophages release pro-inflammatory cytokines and active immune response (Martinez, Abril, Earnest, & Watson, 1992). Those pro-inflammatory cytokines activate NF-κB signalling pathway and then accelerate inflammatory response (Tsan & Gao, 2009).
Transcriptional control of maladaptive and protective responses in alcoholics: A role of the NF-κB system
2011, Brain, Behavior, and ImmunityCitation Excerpt :While both NF-κB function and RelA expression were upregulated shortly after ethanol administration (Rulten et al., 2006), the increase appears to be transient since it is not sustained following sub-chronic ethanol treatment (a 9% ethanol-containing liquid diet for 15 days) (Mittal et al., 1999). Although cellular and molecular mechanisms by which alcohol causes brain damage are not fully understood, numerous studies suggest a role of inflammatory processes (Altura et al., 2002; Blanco et al., 2005; Davis and Syapin, 2004; Lee et al., 2004; Martinez et al., 1992; Minambres et al., 2006; Nelson et al., 1989; Valles et al., 2004). At the transcription level, inflammation is primarily regulated by NF-κB and related factors in a variety of cells and tissues.
Immediate and prolonged effects of alcohol exposure on the activity of the hypothalamic-pituitary-adrenal axis in adult and adolescent rats
2011, Brain, Behavior, and ImmunityCitation Excerpt :Indeed, the ability of LPS to activate PVN CRF neurons further supports this concept (Lee et al., 1995). Furthermore, a review of potential interactions between alcohol and cytokine secretion (Martinez et al., 1992) lead to the concept that alcohol might release cytokines, which led our laboratory to investigate the hypothesis that the stimulatory effect of alcohol on the HPA axis might, at least in part, depend on endogenous cytokine release. In particular, we explored the effects of acute pretreatment with alcohol upon the release of ACTH, corticosterone and pro-inflammatory cytokines (TNFα and IL-6) following endotoxicity (LPS administration), and found that the drug increased the corticosterone, but not the ACTH response to LPS (Rivier, 1999).
Inhibitory effect of osthole on alcohol-induced fatty liver in mice
2009, Digestive and Liver DiseaseCitation Excerpt :Therefore, alcoholic fatty liver should be treated as an important liver disorder. Sensitization of Kupffer cells is a prominent event in the initiation of alcoholic liver disease [3]. Sensitized Kupffer cells are activated by endotoxin (lipopolysaccharide, LPS), leading to a rapid increase in intracellular calcium followed by releases of inflammatory mediators (e.g., cytokines and lipid metabolites [4]), and reactive oxygen species (ROS).
Roles of Kupffer Cells in Alcoholic Liver Disease
2005, Comprehensive Handbook of Alcohol Related PathologyOxidants and antioxidants in alcohol-induced liver disease
2003, GastroenterologyCitation Excerpt :There is accumulating evidence that inappropriate activation of Kupffer cells plays a key role in the initiation of alcohol-induced liver injury.38 Specifically, alcohol primes Kupffer cells and monocytes, increasing phagocytic and bactericidal activities, and cytokine production.39–41 Another major process that is stimulated in primed macrophages/monocytes is the production of prooxidants.