PMID- 23855294
OWN - NLM
STAT- MEDLINE
DCOM- 20140325
LR  - 20211021
IS  - 1440-1746 (Electronic)
IS  - 0815-9319 (Print)
IS  - 0815-9319 (Linking)
VI  - 28 Suppl 1
IP  - 0 1
DP  - 2013 Aug
TI  - Toll-like receptors in alcoholic liver disease, non-alcoholic steatohepatitis and 
      carcinogenesis.
PG  - 38-42
LID - 10.1111/jgh.12019 [doi]
AB  - Activation of innate immune systems including Toll-like receptor (TLR) signaling 
      is a key in chronic liver disease. Recent studies suggest that gut 
      microflora-derived bacterial products (i.e. lipopolysaccharide [LPS], bacterial 
      DNA) and endogenous substances (i.e. high-mobility group protein B1 [HMGB1], free 
      fatty acids) released from damaged cells activate hepatic TLRs that contribute to 
      the development of alcoholic (ASH) and non-alcoholic steatohepatitis (NASH) and 
      liver fibrosis. The crucial role of TLR4, a receptor for LPS, has been implicated 
      in the development of ASH, NASH, liver fibrosis, and hepatocellular carcinoma. 
      However, the role of other TLRs, such as TLR2 and TLR9 in chronic liver disease 
      remains less clear. In this review, we will discuss the role of TLR2, 4, and 9 in 
      Kupffer cells and hepatic stellate cells in the development of ASH, NASH, and 
      hepatocarcinogenesis.
CI  - (c) 2013 Journal of Gastroenterology and Hepatology Foundation and Wiley Publishing 
      Asia Pty Ltd.
FAU - Roh, Yoon Seok
AU  - Roh YS
AD  - Division of Gastroenterology, Department of Medicine, University of California, 
      San Diego, School of Medicine, La Jolla, California 92093-0702, USA.
FAU - Seki, Ekihiro
AU  - Seki E
LA  - eng
GR  - R01AA02172/AA/NIAAA NIH HHS/United States
GR  - R01 AA020172/AA/NIAAA NIH HHS/United States
GR  - P42ES010337/ES/NIEHS NIH HHS/United States
GR  - P42 ES010337/ES/NIEHS NIH HHS/United States
GR  - R01 DK085252/DK/NIDDK NIH HHS/United States
GR  - R01DK085252/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Review
PL  - Australia
TA  - J Gastroenterol Hepatol
JT  - Journal of gastroenterology and hepatology
JID - 8607909
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Toll-Like Receptor 2)
RN  - 0 (Toll-Like Receptor 4)
RN  - 0 (Toll-Like Receptor 9)
SB  - IM
MH  - Animals
MH  - Carcinoma, Hepatocellular/*immunology
MH  - Fatty Liver/*immunology
MH  - Hepatic Stellate Cells/immunology
MH  - Humans
MH  - Kupffer Cells/immunology
MH  - Lipopolysaccharides
MH  - Liver Diseases, Alcoholic/*immunology
MH  - Liver Neoplasms/*immunology
MH  - Mice
MH  - Myeloid Differentiation Factor 88/immunology/physiology
MH  - Non-alcoholic Fatty Liver Disease
MH  - Signal Transduction/immunology/physiology
MH  - Toll-Like Receptor 2/immunology/*physiology
MH  - Toll-Like Receptor 4/immunology/*physiology
MH  - Toll-Like Receptor 9/immunology/*physiology
PMC - PMC3721430
MID - NIHMS417112
OTO - NOTNLM
OT  - LPS
OT  - MyD88
OT  - TLR4
OT  - intestinal microflora
OT  - liver fibrosis
COIS- Conflicts of interest: There is no conflict of interest to disclose for all 
      authors.
EDAT- 2013/07/24 06:00
MHDA- 2014/03/26 06:00
PMCR- 2014/08/01
CRDT- 2013/07/17 06:00
PHST- 2012/10/31 00:00 [accepted]
PHST- 2013/07/17 06:00 [entrez]
PHST- 2013/07/24 06:00 [pubmed]
PHST- 2014/03/26 06:00 [medline]
PHST- 2014/08/01 00:00 [pmc-release]
AID - 10.1111/jgh.12019 [doi]
PST - ppublish
SO  - J Gastroenterol Hepatol. 2013 Aug;28 Suppl 1(0 1):38-42. doi: 10.1111/jgh.12019.