Open AccessReduced host resistance and Th1 response to Cryptococcus neoformans in interleukin‐18 deficient mice
Author(s) -
Kawakami Kazuyoshi,
Koguchi Yoshinobu,
Qureshi Mahboob Hossain,
Kinjo Yuki,
Yara Satomi,
Miyazato Akiko,
Kurimoto Masashi,
Takeda Kiyoshi,
Akira Shizuo,
Saito Atsushi
Publication year - 2000
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2000.tb09092.x
Subject(s) - cryptococcus neoformans , spleen , biology , interferon gamma , stimulation , microbiology and biotechnology , cytokine , ratón , immunology , immune system , interleukin 4 , interleukin , endocrinology
Using interleukin (IL)‐18 deficient (IL‐18 −/− ) mice, we examined the role of IL‐18 in the host resistance and Th1 response against infection with Cryptococcus neoformans . Fungal clearance in the lung was reduced in IL‐18 −/− mice, although there was no significant change in the level of dissemination to the brain. The DTH response, as determined by footpad swelling, was also diminished in IL‐18 −/− mice compared to control wild‐type (WT) mice. The levels of IL‐12 and interferon (IFN)‐γ in the sera were significantly lower in IL‐18 −/− mice than in WT mice. Spleen cells from infected WT mice produced a high level of IFN‐γ upon stimulation with the microbe, while only a low level of IFN‐γ production was detected in spleen cells from infected IL‐18 −/− mice. Administration of IL‐18 almost completely restored the reduced response in IL‐18 −/− mice, while IL‐12 showed a marginal effect. These results demonstrated the important role of IL‐18 in the resistance and Th1 response of mice to C. neoformans by potentiating the production of IFN‐γ.