Effect of Ultraviolet B Irradiation on the TNF-alpha /IFN-gamma Production and Immunity to Listeria monocytogenes Infection in Mice.
- Author:
Suhn Young IM
;
Hyun Chul LEE
;
In Chol KANG
;
Keong A RHO
;
Soon Bai CHUN
;
Hwang Hee Blasie LEE
;
Chun Sang KIM
- Publication Type:Original Article
- MeSH:
Adaptive Immunity;
Animals;
Cytokines;
Depression;
Immunity, Cellular;
Immunity, Innate;
Immunization;
Listeria monocytogenes*;
Listeria*;
Macrophages;
Macrophages, Peritoneal;
Mice*;
Spleen;
Streptomycin;
Tumor Necrosis Factor-alpha*
- From:Journal of the Korean Society for Microbiology
1997;32(5):581-592
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The ultraviolet radiation (UVR) is known to be a potent modulator of many host immune functions and the exposure of experimental animals to the inflammatory effects of UVR induces depressions in their ability to initiate and effectuate various types of cellular immune responses. In this study, the effects of UV-B (280 320 nm) radiation on resistance to a facultative intracellular bacterium, Listeria monocytogenes (LM), were examined at the cellular level. The numbers of cultivable LM recovered from the spleens of UV-B-irradiated mice were decreased at 2 days postinfection compared with those of untreated control mice. However, the acquired immunity, developed 7 days after immunization with streptomycin (SM)-sensitive LM, in either UV-irradiated, LPS- or IL-1-pretreated mice was less stronger than that developed in untreated, control mice. To elucidate the possible mechanisms underlying the observation that UVR did increase innate immunity but decreased acquired immunity of mice to the infection with LM, the effects of UVR of mice on the production of IFN-r by activated splenocytes and TNF-a by peritoneal macrophages were assessed. Activated splenocytes from UV-irradiated mice exhibited a reduced capacity to produce IFN-r and cultured peritoneal macrophages produced more TNF-a in the presence of LPS during 24 hours after UV radiation. Though TNF-r activity was not detected in the sera of LM-infected mice, intravenous LPS injection induced TNF-r production and UVR decreased TNF activity in sera obtained from LM-infected mice with LPS induction 9 days after irradiation. Although Ia-negative macrophages were predominant in the peritoneal macrophages from untreated control mice, the infection of mice with LM caused a marked increase in Ia expression on peritoneal macrophages. However, UVR resulted in decreased expression of Ia molecule on the peritoneal macrophages during the LM infection. These findings suggest that the dual effects of UVR on the innate and acquired immunity of mice to the LM infection may be associated with altered capacities of splenocytes and peritoneal macrophages of the mice to produce cytokines, in addition to decrease of la molecule expression on the macrophages.
