Open AccessVirus‐vs endotoxin‐induced activation of liver macrophages
Author(s) -
BUSAM Klaus Johannes,
HOMFELD Angela,
ZAWATZKY Rainer,
KÄSTNER Stefanie,
BAUER Joachim,
GEROK Wolfgang,
DECKER Karl
Publication year - 1990
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1990.tb19160.x
Subject(s) - sendai virus , virus , tumor necrosis factor alpha , stimulation , macrophage , newcastle disease , interferon , prostaglandin e2 , interleukin , biology , lipopolysaccharide , virology , microbiology and biotechnology , immunology , chemistry , cytokine , endocrinology , in vitro , biochemistry
The response of liver macrophages (Kupffer cells) to distinct pathogenic material was investigated by comparing virus‐ and endotoxin‐induced macrophage activation. Endotoxin‐induced stimulation and induction with Newcastle disease virus (NDV) or Sendai virus led to the release of the same pattern of prostanoids characterized by a predominant production of prostaglandin E 2 (PGE 2 ). With respect to peptide mediators, hepatic macrophages secreted tumor necrosis factor‐α (TNF‐α) and interleukin‐6 after viral induction and endotoxin treatment, respectively. In response to viruses, however, much more interleukin‐6 and TNF‐α was detected than after endotoxin stimulation. Interferon type I (interferon‐α/β), on the other hand, was only detected in the supernatants of macrophages infected with viruses, but not of those exposed to endotoxin. This study also revealed that rat TNF‐α exists in several soluble species, some of which are glycosylated.