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Cytokine‐induced neutrophil chemoattractant release from hepatocytes is modulated by Kupffer cells
Author(s) -
Mawet E,
Shiratori Y,
Hikiba Y,
Takada H,
Yoshida H,
Okano K,
Komatsu Y,
Matsumura M,
Niwa Y,
Omata M
Publication year - 1996
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510230223
Subject(s) - kupffer cell , cytokine , tumor necrosis factor alpha , collagenase , chemotaxis , neutrophile , biology , microbiology and biotechnology , messenger rna , liver injury , liver cytology , interleukin 8 , hepatocyte , interleukin , chemistry , inflammation , in vitro , endocrinology , immunology , enzyme , biochemistry , receptor , liver metabolism , gene
To clarify the role of intercellular communication in the liver during accumulation of neutrophils, the release of cytokine‐induced neutrophil chemoattractant (CINC) (interleukin‐8 [IL‐8] related protein in rodents) by hepatocytes was investigated in the presence of Kupffer cell‐conditioned medium in vitro . Kupffer cells were prepared by perfusion of rat liver with collagenase followed by centrifugation on a metrizamide gradient and were cultured in the presence or absence of lipopolysacharide (LPS). The conditioned medium was collected after 24 hours, and rat hepatocytes were cultured in the presence or absence of Kupffer cell‐conditioned medium. An amount of CINC in the culture supernatant was measured by western blotting analysis and enzyme‐linked immunosorbent assay (ELISA), and expression of its messenger RNA (mRNA) was assessed by the polymerase chain reaction. LPS‐stimulated Kupffer cell‐conditioned medium enhanced an expression of CINC mRNA in hepatocytes and increased the production of CINC by hepatocytes. Enhanced production of CINC was not shown when the Kupffer cell‐conditioned medium was pretreated with heat (56 degrees C, 30 minutes). The production of CINC by hepatocytes in the presence of the LPS‐stimulated Kupffer cell‐conditioned medium was reduced by an antibody against interleukin 1β (IL‐1β), but not by antibodies against tumor necrosis factor α (TNF‐α) or LPS. These results suggest that production of CINC by hepatocytes could be regulated by IL‐1β released from Kupffer cells, leading to neutrophil accumulation during liver injury, because this protein is a strong chemoattractant for neutrophils.