UV-B irradiation increases susceptibility of mice to malarial infection

被引:19
作者
Yamamoto, K
Ito, R
Koura, M
Kamiyama, T
机构
[1] Natl Inst Infect Dis, Dept Virol 1, Shinjuku Ku, Tokyo 1628640, Japan
[2] Natl Inst Infect Dis, Dept Vet Sci, Shinjuku Ku, Tokyo 1628640, Japan
关键词
D O I
10.1128/IAI.68.4.2353-2355.2000
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
We here examined whether exposure of mice to UV-B affected their susceptibility to the murine malaria parasite Plasmodium chabaudi. When BALB/c mice with depilated skin were irradiated with W-B and subsequently infected with the parasite, 80 to 100% of the UV-B-irradiated mice died within 12 days of infection with a sublethal dose. In addition, UV-B irradiation of C57BL/10 (B-10) mice, which are otherwise naturally resistant to the parasites, rendered them susceptible, and 100% of irradiated B-10 mice died within 11 days postinfection. The level of plasma gamma interferon (IFN-gamma) in unirradiated B-10 mice at 5 days after infection increased to 566 pg/ml, whereas the UV-B exposure of mice impaired the production of IFN-gamma, which showed a maximum level of 65 pg/ml in response to the parasite infection. The maximum level of plasma interleukin-10 in UV-B-irradiated mice in response to the parasite infection was similar to 1,100 pg/ml, which was approximately fourfold higher than the maximum level in unirradiated control mice. When UV-B-irradiated B-10 mice were administered murine recombinant IFN-gamma after infection, the mice regained parasite resistance. These results demonstrated that the UV-B exposure of mice enhances the susceptibility to the malaria parasites and suggested that the enhanced susceptibility following UV-B exposure was mediated by impairment of IFN-gamma production in response to the parasite infection.
引用
收藏
页码:2353 / 2355
页数:3
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