PMID- 31102558
OWN - NLM
STAT- MEDLINE
DCOM- 20200520
LR  - 20201001
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 198
IP  - 1
DP  - 2019 Oct
TI  - IL-17 and TNF-alpha co-operation contributes to the proinflammatory response of 
      hepatic stellate cells.
PG  - 111-120
LID - 10.1111/cei.13316 [doi]
AB  - Hepatic stellate cells (HSCs) have a central role in liver inflammation and 
      fibrosis by producing inflammatory and fibrotic mediators. Their activation is 
      regulated through direct cell-cell interactions, but also through systemic and 
      local effects of soluble factors such as cytokines. The effects of the 
      proinflammatory cytokines interleukin (IL)-17 and tumor necrosis factor (TNF)-alpha 
      and cell interactions with hepatocytes on HSC activation were assessed. Human HSC 
      and HepaRG cells were exposed to IL-17 and/or TNF-alpha. IL-17 and TNF-alpha contribution 
      from immune cells was determined in a co-culture model with phytohemagglutinin 
      (PHA)-activated peripheral blood mononuclear cells (PBMC), HSC and/or 
      hepatocytes. IL-17 enhanced TNF-alpha effects on the induction of IL-6, IL-1beta, and 
      the chemokine IL-8, chemokine (C-C motif) ligand 20 (CCL20) and monocyte 
      chemoattractant protein-1 (MCP-1) expression/secretion in isolated HSC cultures. 
      HSC-hepatocyte interactions did not enhance IL-6, IL-8 and CCL20 production 
      compared to hepatocyte alone. However, HSC-hepatocyte interactions increased 
      C-reactive protein expression. IL-17 and/or TNF-alpha had no direct profibrotic 
      effects on collagen 1 alpha1, tissue inhibitor of matrix metalloproteinase (TIMP) and 
      matrix metalloproteinase (MMP) 2 gene expression, whereas mRNA levels of MMP3, an 
      enzyme involved in matrix destruction, were up-regulated in HSCs. The use of 
      specific inhibitors of IL-17 and TNF-alpha indicated their contribution to the strong 
      increase of IL-6 and IL-8 production induced by PBMC, HSC and/or hepatocyte 
      interactions. As chronic liver inflammation leads to liver fibrosis, IL-17 and/or 
      TNF-alpha neutralization can be of interest to control liver inflammation and 
      therefore its effects on fibrosis.
CI  - (c) 2019 British Society for Immunology.
FAU - Beringer, A
AU  - Beringer A
AD  - Immunogenomics and Inflammation research Unit EA 4130, University of Lyon, Lyon, 
      France.
AD  - Department of Clinical Immunology and Rheumatology, Hospices Civils de Lyon, 
      Lyon, France.
FAU - Miossec, P
AU  - Miossec P
AUID- ORCID: 0000-0002-3280-6346
AD  - Immunogenomics and Inflammation research Unit EA 4130, University of Lyon, Lyon, 
      France.
AD  - Department of Clinical Immunology and Rheumatology, Hospices Civils de Lyon, 
      Lyon, France.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190606
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL20)
RN  - 0 (Collagen Type I)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-17)
RN  - 0 (Tissue Inhibitor of Metalloproteinase-1)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Chemokine CCL20/metabolism
MH  - Collagen Type I/metabolism
MH  - Cytokines/metabolism
MH  - Hepatic Stellate Cells/*metabolism
MH  - Hepatocytes/metabolism
MH  - Humans
MH  - Inflammation/*metabolism
MH  - Interleukin-17/*metabolism
MH  - Leukocytes, Mononuclear/metabolism
MH  - Liver/metabolism
MH  - Liver Cirrhosis/metabolism
MH  - Tissue Inhibitor of Metalloproteinase-1/metabolism
MH  - Tumor Necrosis Factor-alpha/*metabolism
PMC - PMC6718275
OTO - NOTNLM
OT  - cell interactions
OT  - hepatic stellate cells
OT  - inflammation
OT  - interleukin-17
OT  - tumor necrosis factor-alpha
COIS- None.
EDAT- 2019/05/19 06:00
MHDA- 2020/05/21 06:00
PMCR- 2020/10/01
CRDT- 2019/05/19 06:00
PHST- 2019/05/13 00:00 [accepted]
PHST- 2019/05/19 06:00 [pubmed]
PHST- 2020/05/21 06:00 [medline]
PHST- 2019/05/19 06:00 [entrez]
PHST- 2020/10/01 00:00 [pmc-release]
AID - CEI13316 [pii]
AID - 10.1111/cei.13316 [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2019 Oct;198(1):111-120. doi: 10.1111/cei.13316. Epub 2019 Jun 
      6.