Experimental study of antibiotic-induced immunosuppression in mice. II. Th, Ts and NC cell involvement.

In penicillin(pen), streptomycin(str), kanamycin(kan) and tetracycline(tet)-treated CBA/J adult mice, no difference was noticed as concerned spleen T "helper" (Th) cell activity, as studied by means of response to PHA of X-irradiated/whole T fraction cell mixtures in vitro. On the contrary, in erythromycin(erm), colistin(col) and chloramphenicol(chl)-treated groups, Th cell activity was significantly decreased. On the other hand, spleen T "suppressor" (Ts) cell activity (assayed by response to PHA of mixtures containing pre-incubated with Concanavalin A and whole T cells, respectively) was augmented in samples arising from chl-treated group. These results are also supported by experiments testing Th or Ts soluble factors, induced in spleen T cells belonging to each antibiotic-treated group and purified by affinity chromatography (Concanavalin A-Sepharose 4B columns). Thus, it was confirmed both Th cell deficiency in erm, col or chl-groups, and Ts cell augmentation in chl-group. As regards spleen "natural cytotoxic" (NC) cell activity, as tested in a xenogeneic "target" cell substrate, a diminished cytotoxic capacity manifested chl-group-derived NC cells, possibly by richness in own "non-specific suppressor" (NSS) cells. NC cell samples in vitro supplemented with NSS cells arising from suckling mouse spleens and a lower cytotoxic activity, in a larger extent in chl-group-derived NC cells, as compared to other groups. The pre-incubation of control-group-NC cells with several antibiotic preparations in vitro was followed by decrease of the cytotoxic values in erm, col and chl-samples, suggesting a drug-induced NC receptor "masking", that prevented "target" cell recognition in mice--II. In the case of NSS addition in vitro, as strong inhibition of the cytotoximity occurred in chl-treated NC cells derived from the control group, that proves a possible chloramphenicol-induced immunodepression by potentiation of NSS inhibitory effect on NC cells. Based upon data from the present work, as well as from the previous work, the authors suggest a classification of several mechanisms by which the antibacterial antibiotics can act as immunosuppressive.