抄録
We previously established a system for induction of mucosal-type mast cells from mouse spleen cells by long-term culture without exogenous interleukin 3 (IL-3) . Fetal calf serum (FCS) was important and could be divided into mast cell-inducible and non-mast cell-inducible sera. Lipopolysaccharide (LPS) -contaminating FCS was responsible for mast cell induction. Further experiments revealed that IL-3 alone could not induce mast cells, and that mast cell induction by LPS was mediated through endogenous IL-3 and prostaglandin E (PGE) . However, it is not clear whether LPS from various gram-negative bacteria, polysaccharides, and muramyl dipeptide (MDP) are able to induce mast cells. In the present study, LPS from Escherichia coli, Vibrio cholerae, Salmonella Typhinmurium, and Rhodobacter sphaeroides and synthetic lipid A induced mast cells, although higher concentrations of LPS from Rhodobacter sphaeroides were necessary. Polysaccharides (schizophyllan and mannoglucan) from fungi and actinomyces induced mast cells in a dose-dependent and a molecular weight-dependent manner. However, MDP of Mycobacterium tuberculosis failed to induce mast cells. Mast cell induction by the polysaccharides was not due to LPS contamination, since polymyxin B did not suppress the action of the poly-saccharides. Indomethacin, a selective inhibitor for PGE synthesis, suppressed mast cell induction by the polysaccharides. This finding indicates that mast cell induction by the polysaccharides is also mediated through endogenous PGE.
