Suppression of delayed-type hypersensitivity mediated by macrophage-like cells in mice with experimental liver injury.

The intensity of picryl chloride-induced delayed-type hypersensitivity (PCl-DTH) was significantly lowered in mice with experimental liver injury induced by the injection of carbon tetrachloride (CCl4) or 1-naphthylisothiocyanate (ANIT). Adherent spleen cells prepared from mice with liver injury suppressed the PCl-DTH in normal syngeneic mice by adoptive transfer at the time of immunization with picryl chloride (PCl). Cianidanol, administered orally to recipient mice immediately after the transfer of adherent spleen cells, caused total prevention of the PCl-DTH from suppression by the transferred adherent spleen cells. In in vitro studies, the adherent spleen cells from both CCl4-treated and ANIT-treated mice produced higher amounts of prostaglandin E2 (PGE2) than those from normal mice. The addition of cianidanol at the beginning of incubation caused an inhibition of PGE2 production of the adherent spleen cells. Furthermore, the spleen cell suspensions from CCl4-treated mice gave a marked increase in generation of superoxide anions (O2-), also inhibited by the addition of cianidanol. Gathered results support the adherent spleen cell as being the cell causing the suppression of DTH in mice with experimental liver injury; the important role of PGE2 and O2- in the suppression of DTH mediated by the adherent spleen cells was demonstrated. Cianidanol eliminated the suppression of DTH, owing principally to the inhibitory effect on the production of PGE2 and O2- from the adherent spleen cells.