CANDIDA-SPECIFIC TH1-TYPE RESPONSIVENESS IN MICE WITH EXPERIMENTAL VAGINAL CANDIDIASIS
CANDIDA-SPECIFIC TH1-TYPE RESPONSIVENESS IN MICE WITH EXPERIMENTAL VAGINAL CANDIDIASIS
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DOI：
10.1128/iai.61.10.4202-4207.1993
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发表时间：
1993-10-01
影响因子：
3.1
通讯作者：
SOBEL, JD
中科院分区：
文献类型：
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作者：
FIDEL, PL;LYNCH, ME;SOBEL, JD
系统性细胞介导免疫（CMI）作为阴道中宿主防御机制的作用知之甚少。使用小鼠假动情模型的实验性阴道念珠菌病，我们以前发现，动物阴道接种的活白色念珠菌芽生孢子获得了持续的阴道感染，并制定了念珠菌特异性迟发型超敏反应（DTH）。本研究旨在表征小鼠阴道感染产生的外周CMI反应性，并确定假发情是否是诱导外周CMI反应性的先决条件。用雌激素处理或未处理的小鼠，阴道接种C。白念珠菌芽生分生孢子检测4周，检测其阴道念珠菌负荷和外周CMI反应性，包括DTH反应性和体外应答念珠菌抗原的Th 1（白细胞介素-2 [IL-2]，γ干扰素[IFN-γ]）/Th 2（IL-4，IL-10）型淋巴因子产生。结果表明，尽管小鼠在阴道接种C。白色念珠菌芽生分生孢子仅发展为短暂的阴道感染，并且与给予雌激素然后感染的那些相比，阴道中的念珠菌CFU显著更少; DTH反应性在两组中相等。CMI反应性的体外测量进一步表明，在阴道接种后4周内，来自雌激素和非雌激素治疗的感染小鼠的淋巴结细胞产生升高水平的IL-2和IFN-γ以响应念珠菌抗原。相比之下，来自相同阴道感染小鼠的淋巴结细胞在感染的第4周期间显示没有IL-10产生并且仅IL-4小幅升高。这些结果表明，实验性阴道念珠菌病的小鼠主要是Th 1型念珠菌特异性外周CMI反应性和类似的模式，Th 1型反应性发生在小鼠中，无论感染的持续性和雌激素状态的感染小鼠。
The role of systemic cell-mediated immunity (CMI) as a host defense mechanism in the vagina is poorly understood. Using a murine pseudoestrus model of experimental vaginal candidiasis, we previously found that animals given a vaginal inoculum of viable Candida albicans blastoconidia acquired a persistent vaginal infection and developed Candida-specific delayed-type hypersensitivity (DTH) responses. The present study was designed to characterize the peripheral CMI reactivity generated from the vaginal infection in mice and to determine whether pseudoestrus is a prerequisite for the induction of peripheral CMI reactivity. Mice treated or not treated with estrogen and given a vaginal inoculum of C. albicans blastoconidia were examined for 4 weeks for their vaginal Candida burden and peripheral CMI reactivity, including DTH responsiveness and in vitro Th1 (interleukin-2 [IL-2], gamma interferon [IFN-gamma])/Th2 (IL-4, IL-10)-type lymphokine production in response to Candida antigens. Results showed that although mice not treated with estrogen before being given a vaginal inoculum of C. albicans blastoconidia developed only a short-lived vaginal infection and harbored significantly fewer Candida CFU in the vagina compared with those given estrogen and then infected; DTH reactivity was equivalent in both groups. In vitro measurement of CMI reactivity further showed that lymph node cells from both estrogen- and non-estrogen-treated infected mice produced elevated levels of IL-2 and IFN-gamma in response to Candida antigens during the 4 weeks after vaginal inoculation. In contrast, lymph node cells from the same vaginally infected mice showed no IL-10 production and only small elevations of IL-4 during week 4 of infection. These results suggest that mice with experimental vaginal candidiasis develop predominantly Th1-type Candida-specific peripheral CMI reactivity and that similar patterns of Th1-type reactivity occur in mice regardless of the persistence of infection and the estrogen status of the infected mice.