Alteration of radioprotective effects of heat-killed Lactobacillus casei in X-irradiated C3H/He mouse related to blood level of proinflammatory cytokines by corticoids.

It is well known that a pre-administration of proinflammatory cytokines alters hematopoietic progenitor cells to promote an increase resistance against radiation and increases the survival rate in mice irradiated with lethal doses of radiation. Inflammation stimulators, such as some bacterial constituents, are also reported to have similar radioprotective action. We found that pre-administration of heat-killed Lactobacillus casei (HLC) to mice increases the level of interleukin (IL)-1 beta in circulation as well as the survival rate following lethal dose of radiation. Since HLC stimulates early immune responses, effects by drugs to modify inflammation were studied. The increase of both blood IL-1 beta levels and survival rates by HLC were simultaneously accelerated by coadministration of mineralocorticoid and inhibited by glucocorticoids or corticotropin. Neither parameter was modified by non-steroidal anti-inflammatory or anti-rheumatoid drugs. This suggests that both expected radioprotective action and unexpected systemic action, realized as an increase in plasma cytokines, by inflammation-related radioprotectors can be controlled by the coadministration of drugs at least in C3H/He mice, based on consideration of their pharmacological properties.