Show simple item record

dc.contributor.authorGao, Bin
dc.contributor.authorSeki, Ekihiro
dc.contributor.authorCohen, Jessica
dc.contributor.authorNagy, Laura
dc.contributor.authorSzabo, Gyongyi
dc.contributor.authorZakhari, Samir
dc.date2022-08-11T08:08:37.000
dc.date.accessioned2022-08-23T16:01:38Z
dc.date.available2022-08-23T16:01:38Z
dc.date.issued2011-01-22
dc.date.submitted2011-03-09
dc.identifier.citationAmerican journal of physiology. Gastrointestinal and liver physiology. 2011 Jan 20. <a href="http://dx.doi.org/10.1152/ajpgi.00537.2010">Link to article on publisher's site</a>
dc.identifier.issn0193-1857 (Linking)
dc.identifier.doi10.1152/ajpgi.00537.2010
dc.identifier.pmid21252049
dc.identifier.urihttp://hdl.handle.net/20.500.14038/31176
dc.description.abstractExcessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, while activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates the complement system in the liver by yet unidentified mechanisms, leading to alcoholic steatohepatitis. In contrast to activation of TLR4 and complement, alcohol consumption can inhibit natural killer cells, another important innate immunity component, contributing to alcohol acceleration of viral infection and liver fibrosis in patients with chronic viral hepatitis. Understanding of the role of innate immunity in the pathogenesis of alcoholic liver disease may help us identify novel therapeutic targets to treat this disease.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=21252049&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1152/ajpgi.00537.2010
dc.subjectLiver Diseases, Alcoholic
dc.subjectImmunity, Innate
dc.subjectGastroenterology
dc.titleInnate immunity and alcoholic liver disease
dc.typeJournal Article
dc.source.journaltitleAmerican journal of physiology. Gastrointestinal and liver physiology
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gastroenterology_pp/99
dc.identifier.contextkey1862017
html.description.abstract<p>Excessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, while activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates the complement system in the liver by yet unidentified mechanisms, leading to alcoholic steatohepatitis. In contrast to activation of TLR4 and complement, alcohol consumption can inhibit natural killer cells, another important innate immunity component, contributing to alcohol acceleration of viral infection and liver fibrosis in patients with chronic viral hepatitis. Understanding of the role of innate immunity in the pathogenesis of alcoholic liver disease may help us identify novel therapeutic targets to treat this disease.</p>
dc.identifier.submissionpathgastroenterology_pp/99
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology


This item appears in the following Collection(s)

Show simple item record