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全身性念珠菌病对无菌和常规大鼠淋巴细胞增殖的影响。

Effect of systemic candidiasis on blastogenesis of lymphocytes from germfree and conventional rats.

作者信息

Rogers T J, Balish E

出版信息

Infect Immun. 1978 Apr;20(1):142-50. doi: 10.1128/iai.20.1.142-150.1978.

Abstract

Germfree and conventional rats were challenged (intravenously) with Candida albicans and sacrificed at various times after infection, and their spleen cells were harvested to examine the effect of disseminated candidiasis on in vitro lymphocyte hypersensitivity to Candida antigens (CA). Results showed that conventional rat splenocytes, initially responsive in vitro to stimulation by CA, manifested a depression in CA-specific responsiveness after challenge with viable C. albicans (days 3 to 6 postchallenge). In addition, the latter splenocyte response to phytohemagglutinin (PHA) and concanavalin A (ConA) was suppressed by 3 to 6 days after challenge with Candida. In contrast to conventional rats, the response of germfree rat splenocytes to CA was insignificant before challenge with C. albicans, and it was increased at 9 days after infection. The response of uninfected germfree rat splenocytes to PHA and ConA was significantly lower than that of unchallenged conventional rats. Challenge with viable C. albicans did not result in a suppression of gnotobiotic rat splenocyte responses to PHA and ConA, but rather, the disseminated infection resulted in as much as fivefold increases in PHA or ConA-induced blastogenesis. These findings suggest that disseminated candidiasis is capable of suppressing blastogenesis in immunologically mature conventional rats and of improving lymphocyte blastogenesis from immunologically immature germfree rats.

摘要

将无菌大鼠和普通大鼠静脉注射白色念珠菌进行感染,并在感染后的不同时间点处死,采集它们的脾细胞,以研究播散性念珠菌病对体外淋巴细胞对念珠菌抗原(CA)超敏反应的影响。结果显示,普通大鼠的脾细胞最初在体外对CA刺激有反应,但在用活的白色念珠菌攻击后(攻击后3至6天),其对CA的特异性反应性出现下降。此外,在用念珠菌攻击后3至6天,后者的脾细胞对植物血凝素(PHA)和刀豆蛋白A(ConA)的反应受到抑制。与普通大鼠不同,无菌大鼠的脾细胞在受到白色念珠菌攻击之前对CA的反应不明显,而在感染后9天反应增强。未感染的无菌大鼠脾细胞对PHA和ConA的反应明显低于未受攻击的普通大鼠。用活的白色念珠菌攻击不会导致无菌大鼠脾细胞对PHA和ConA的反应受到抑制,相反,播散性感染导致PHA或ConA诱导的母细胞形成增加多达五倍。这些发现表明,播散性念珠菌病能够抑制免疫成熟的普通大鼠的母细胞形成,并能改善免疫未成熟的无菌大鼠的淋巴细胞母细胞形成。

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