PMID- 26576079
OWN - NLM
STAT- MEDLINE
DCOM- 20161031
LR  - 20181113
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 21
IP  - 42
DP  - 2015 Nov 14
TI  - Immune dysfunction in acute alcoholic hepatitis.
PG  - 11904-13
LID - 10.3748/wjg.v21.i42.11904 [doi]
AB  - Acute alcoholic hepatitis (AAH) is a serious complication of alcohol misuse and 
      has high short term mortality. It is a clinical syndrome characterised by 
      jaundice and coagulopathy in a patient with a history of recent heavy alcohol use 
      and is associated with profound immune dysfunction with a primed but ineffective 
      immune response against pathogens. Here, we review the current knowledge of the 
      pathogenesis and immune defects of AAH and identify areas requiring further 
      study. Alcohol activates the immune system primarily through the disruption of 
      gut tight junction integrity allowing the escape of pathogen-associated molecular 
      particles (PAMPs) into the portal venous system. PAMPs stimulate cells expressing 
      toll-like receptors (mainly myeloid derived cells) and initiate a network of 
      intercellular signalling by secretion of many soluble mediators including 
      cytokines and chemokines. The latter coordinates the infiltration of neutrophils, 
      monocytes and T cells and results in hepatic stellate cell activation, cellular 
      damage and hepatocyte death by necrosis or apoptosis. On the converse of this 
      immune activation is the growing evidence of impaired microbial defence. 
      Neutrophils have reduced phagocytic capacity and oxidative burst and there is 
      recent evidence that T cell exhaustion plays a role in this.
FAU - Dhanda, Ashwin D
AU  - Dhanda AD
AD  - Ashwin D Dhanda, Peter L Collins, School of Clinical Sciences, University of 
      Bristol, BS2 8HW Bristol, United Kingdom.
FAU - Collins, Peter L
AU  - Collins PL
AD  - Ashwin D Dhanda, Peter L Collins, School of Clinical Sciences, University of 
      Bristol, BS2 8HW Bristol, United Kingdom.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Chemokines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Toll-Like Receptors)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
SB  - IM
MH  - Acute Disease
MH  - Alcohol Drinking/*adverse effects/mortality
MH  - Animals
MH  - Bacterial Translocation
MH  - Chemokines/immunology
MH  - Granulocyte Colony-Stimulating Factor/immunology
MH  - Hepatitis, Alcoholic/diagnosis/*immunology/microbiology/mortality
MH  - Humans
MH  - Immunity, Mucosal
MH  - Inflammation Mediators/immunology
MH  - Intestines/immunology/microbiology
MH  - Liver/*immunology/pathology
MH  - Prognosis
MH  - Risk Factors
MH  - Signal Transduction
MH  - Th17 Cells/immunology
MH  - Toll-Like Receptors/immunology
PMC - PMC4641112
OTO - NOTNLM
OT  - Alcoholic hepatitis
OT  - Alcoholic liver disease
OT  - Gut dysbiosis
OT  - T cell exhaustion
OT  - Toll-like receptors
EDAT- 2015/11/18 06:00
MHDA- 2016/11/01 06:00
PMCR- 2015/11/14
CRDT- 2015/11/18 06:00
PHST- 2015/04/13 00:00 [received]
PHST- 2015/06/03 00:00 [revised]
PHST- 2015/09/30 00:00 [accepted]
PHST- 2015/11/18 06:00 [entrez]
PHST- 2015/11/18 06:00 [pubmed]
PHST- 2016/11/01 06:00 [medline]
PHST- 2015/11/14 00:00 [pmc-release]
AID - 10.3748/wjg.v21.i42.11904 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2015 Nov 14;21(42):11904-13. doi: 
      10.3748/wjg.v21.i42.11904.