PMID- 9875144
OWN - NLM
STAT- MEDLINE
DCOM- 19990114
LR  - 20090929
IS  - 0022-3417 (Print)
IS  - 0022-3417 (Linking)
VI  - 186
IP  - 1
DP  - 1998 Sep
TI  - Distinct patterns of chemokine expression are associated with leukocyte 
      recruitment in alcoholic hepatitis and alcoholic cirrhosis.
PG  - 82-9
AB  - Alcoholic liver disease is associated with three histologically distinct 
      processes: steatosis (parenchymal fat accumulation), alcoholic hepatitis 
      (characterized by parenchymal infiltration by neutrophil polymorphs), and 
      alcoholic cirrhosis (in which chronic inflammation and fibrosis dominate). 
      Chemokines are cytokines that promote subset-specific leukoycte recruitment to 
      tissues and could therefore play a crucial role in determining which leukocyte 
      subsets are recruited to the liver in alcoholic liver disease. This paper reports 
      that chemokine expression is increased in the liver of patients with alcoholic 
      liver disease and, moreover, that distinct patterns of chemokine expression are 
      associated with the different inflammatory responses to alcohol. Interleukin-8 
      (IL-8), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory 
      protein-1 alpha (MIP-1 alpha), and MIP-1 beta were all detected in the parenchyma 
      at sites of inflammation in alcoholic hepatitis, whereas in alcoholic cirrhosis, 
      chemokines were restricted to inflammatory cells and endothelium in the fibrous 
      septa and portal tracts. In alcoholic hepatitis, chemokine transcription was 
      localized to sinusoidal cells, leukocytes, and fibroblasts in areas of 
      parenchymal inflammation, but hepatocytes, despite staining strongly for 
      chemokine protein, were negative. In alcoholic cirrhosis, chemokine mRNA was 
      detected in portal tract endothelium, leukocytes, and fibroblasts. Thus, 
      alcoholic hepatitis and alcoholic cirrhosis are associated with distinct patterns 
      of chemokine expression that are likely to be important factors in determining 
      whether a patient develops acute parenchymal inflammation and alcoholic 
      hepatitis, or chronic septal inflammation and alcoholic cirrhosis.
FAU - Afford, S C
AU  - Afford SC
AD  - Liver Research Laboratories, University of Birmingham, Edgbaston, U.K.
FAU - Fisher, N C
AU  - Fisher NC
FAU - Neil, D A
AU  - Neil DA
FAU - Fear, J
AU  - Fear J
FAU - Brun, P
AU  - Brun P
FAU - Hubscher, S G
AU  - Hubscher SG
FAU - Adams, D H
AU  - Adams DH
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - J Pathol
JT  - The Journal of pathology
JID - 0204634
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokines)
RN  - 0 (Interleukin-8)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL4
MH  - Chemokines/genetics/*metabolism
MH  - Gene Expression
MH  - Hepatitis, Alcoholic/*immunology
MH  - Humans
MH  - Immunoenzyme Techniques
MH  - In Situ Hybridization
MH  - Interleukin-8/metabolism
MH  - Leukocytes/*immunology
MH  - Liver Cirrhosis, Alcoholic/*immunology
MH  - Macrophage Inflammatory Proteins/metabolism
MH  - RNA, Messenger/genetics
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 1999/01/06 06:50
MHDA- 2000/06/20 09:00
CRDT- 1999/01/06 06:50
PHST- 1999/01/06 06:50 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1999/01/06 06:50 [entrez]
AID - 10.1002/(SICI)1096-9896(199809)186:1<82::AID-PATH151>3.0.CO;2-D [pii]
AID - 10.1002/(SICI)1096-9896(199809)186:1<82::AID-PATH151>3.0.CO;2-D [doi]
PST - ppublish
SO  - J Pathol. 1998 Sep;186(1):82-9. doi: 
      10.1002/(SICI)1096-9896(199809)186:1<82::AID-PATH151>3.0.CO;2-D.