Chinese Journal of Dermatology ›› 2003, Vol. 36 ›› Issue (8): 457-460.

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Effects of Heat-Inactivated Cryptococcus neoformans on an Experimental Murine Model of Meningoencephalitis and on IL-1β,IFN-γand TNF-αExpression on the Brain and Spleen

HUANG Xin, WEN Hai, YAO Zhi-rong, HONG Wei, XU Hong, LIAO Wan-qing   

  1. Department of Dermatology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China
  • Received:2002-09-17 Online:2003-08-15 Published:2003-08-15

Abstract: Objective To investigate the effects of heat-inactivated Cryptococcus neoformans(H-CN)on an experimental murine model of meningoencephalitis and on IL-1β,IFN-γand TNF-αgene expression on the brain and spleen.Methods An experimental murine model of intracerebral infection with C.neoformans was established.Mice were divided into H-CN-treated group and control group.The brain and spleen of two groups were collected to obtain total RNA,and IL-1β,IFN-γ and TNF-αwere detected by RT-PCR method.After intracerebral challenging with lethal doses of C.neoformans,the survival time and colony forming units(cfu)of C.neoformans in the brain of two group were observed.Results The survival time was prolonged,and cfu of C.neoformans were decreased in the brain of H-CN-treated group in comparison with those of control group.Expression of IL-1β was positive,and IFN-γand TNF-αnegative in the brain tissue of H-CN-treated mice;while expression of IL-1β,IFN-γand TNF-αwas all negative in the control mice,as indicated by RT-PCR.Expression of3cytokines,IL-1β,IFN-γand TNF-α was all positive in the spleen tissue of both groups,suggesting that there was no significant difference in the levels of cytokine gene transcripts in both groups.Conclusion These findings suggest that murine resistance to central nervous system infection of C.neoformans be enhanced by intracerebral administration of H-CN,and anti-cryptococcal mechanism probably involves a local cytokine IL-1βelicitated by H-CN in central nerve system.

Key words: Cryptococcus neoformans, Interleukin-1, Tumor necrosis factor, Interferon typeⅡ