Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
1990-4-30
pubmed:abstractText
The liver participates in inflammation via the elaboration of acute phase proteins from hepatocytes in response to IL-1, TNF-alpha, and IL-6/INF-beta 2/hepatocyte-stimulating factor. In addition, some inflammatory states of the liver are characterized by leukocyte infiltrates. Here we demonstrate that human hepatocyte lines are capable of expressing mRNA and biologic activity for a neutrophil chemotactic factor (NCF)/IL-8 in response to the inflammatory mediators IL-1 alpha, IL-1 beta, and TNF. Two human hepatoma cell lines (SK-Hep and Hep-G2) displayed a time- and dose-dependent increase in steady state levels of NCF/IL-8 mRNA and secretion of chemotactic activity in response to TNF and IL-1. Neutralizing antibody to NCF/IL-8 inhibited hepatocyte-derived chemotactic activity by 88%. In contrast to IL-1 and TNF, hepatocytes did not respond to LPS or IL-6 within the time and dose parameters used above. Although the expression of NCF/IL-8 mRNA (1.8 kb) was first detectable between 1 and 2 h poststimulation, significant chemotactic bioactivity was not observed until about 4 h. Heat-inactivated (100 degrees C, 30 min) cytokine failed to induced NCF/IL-8 mRNA synthesis, and cotreatment of cells with cytokine and cycloheximide super-induced NCF/IL-8 mRNA while inhibiting production of bioactivity. Thus, NCF/IL-8 expression is a primary induction phenomenon. Our data demonstrate the stimulus specific induction of NCF/IL-8 in hepatocytes and suggest that cytokine cell-to-cell communication circuits may be important in neutrophil-mediated inflammatory processes in the liver.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2609-13
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:2156928-Biological Factors, pubmed-meshheading:2156928-Blotting, Northern, pubmed-meshheading:2156928-Carcinoma, Hepatocellular, pubmed-meshheading:2156928-Chemotactic Factors, pubmed-meshheading:2156928-Cytokines, pubmed-meshheading:2156928-Dose-Response Relationship, Drug, pubmed-meshheading:2156928-Gene Expression, pubmed-meshheading:2156928-Humans, pubmed-meshheading:2156928-Interleukin-1, pubmed-meshheading:2156928-Interleukin-6, pubmed-meshheading:2156928-Interleukin-8, pubmed-meshheading:2156928-Interleukins, pubmed-meshheading:2156928-Lipopolysaccharides, pubmed-meshheading:2156928-Liver, pubmed-meshheading:2156928-Liver Neoplasms, pubmed-meshheading:2156928-RNA, Messenger, pubmed-meshheading:2156928-Recombinant Proteins, pubmed-meshheading:2156928-Tumor Cells, Cultured, pubmed-meshheading:2156928-Tumor Necrosis Factor-alpha
pubmed:year
1990
pubmed:articleTitle
Cytokine-induced gene expression of a neutrophil chemotactic factor/IL-8 in human hepatocytes.
pubmed:affiliation
Department of Pathology, University of Michigan Medical School, Ann Arbor 48109.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't