TY - JOUR
T1 - Reduced host resistance and Th1 response to Cryptococcus neoformans in interleukin-18 deficient mice
AU - Kawakami, Kazuyoshi
AU - Koguchi, Yoshinobu
AU - Qureshi, Mahboob Hossain
AU - Kinjo, Yuki
AU - Yara, Satomi
AU - Miyazato, Akiko
AU - Kurimoto, Masashi
AU - Takeda, Kiyoshi
AU - Akira, Shizuo
AU - Saito, Atsushi
N1 - Funding Information:
This work was supported in part by a Grant-in-Aid for Science Research (09670292) from the Ministry of Education, Science, Sport and Culture, Japan, by grants from the Ministry of Health and Welfare, Japan, and by the Japan Health Science Foundation. The authors thank Dr. F.G. Issa (Word-Medex, Sydney, Australia) for the careful reading and editing of the manuscript.
PY - 2000/5/1
Y1 - 2000/5/1
N2 - 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. Copyright (C) 2000 Federation of European Microbiological Societies.
AB - 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. Copyright (C) 2000 Federation of European Microbiological Societies.
KW - Cryptococcus neoformans
KW - DTH
KW - IL-12
KW - IL-18
KW - Th1 response
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U2 - 10.1016/S0378-1097(00)00128-2
DO - 10.1016/S0378-1097(00)00128-2
M3 - Article
C2 - 10779723
AN - SCOPUS:0034194888
SN - 0378-1097
VL - 186
SP - 121
EP - 126
JO - FEMS Microbiology Letters
JF - FEMS Microbiology Letters
IS - 1
ER -