Mucosal and disseminated candidiasis in gnotobiotic SCID mice.
Mucosal and disseminated candidiasis in gnotobiotic SCID mice.
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无菌 SCID 小鼠的粘膜和播散性念珠菌病。
DOI：
10.1080/02681219380000161
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Leonard,B
中科院分区：
文献类型：
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作者：
Balish,E;Jensen,J;Warner,T;Brekke,J;Leonard,B
无菌SCID小鼠消化道易感染白色念珠菌。C.大量存活种群（106- 108个菌落形成单位g-1）。在16周的研究中，在不同的时间间隔处死的白念珠菌定殖的SCID小鼠表现出角化上皮表面（舌和胃）的慢性浅表粘膜念珠菌病。尽管连续存在大量的可存活的C.在这些小鼠的肠道中，只有浅表粘膜念珠菌病，没有内源性的进行性播散性念珠菌病。环磷酰胺（100 mg kg−1，腹腔注射）治疗增强了SCID小鼠对粘膜（舌和胃）念珠菌病的易感性。知菌（C.还发现SCID小鼠与免疫活性BALB/c小鼠一样对急性（静脉内激发）肾念珠菌病具有抗性。细菌植物群在消化道的定植似乎增强了SCID小鼠对播散性念珠菌病的抵抗力。这项研究表明，先天性免疫机制（吞噬细胞和/或NK细胞），在功能性T细胞和B细胞的情况下，发挥重要作用的抵抗力的SCID小鼠的粘膜和播散性念珠菌病的内源性（肠道）或急性（静脉内挑战）的起源。
The alimentary tracts of germ-free SCID (severe combined immunodeficient) mice were susceptible to colonization withCandida albicans. Large viable populations (106–108colony forming units g−1) ofC. albicans, in pure culture, were present in all sections of the intestinal tract.Candida-colonized SCID mice, sacrificed at various time intervals over a 16 week study, manifested chronic superficial mucosal candidiasis of keratinized epithelial surfaces (tongue and stomach). Despite the continuous presence of large viable populations ofC. albicansin their intestinal tract, only superficial mucosal candidiasis and no progressive disseminated candidiasis of endogenous origin was evident in these mice. Treatment with cyclophosphamide (100 mg kg−1, intraperitoneally) enhanced the susceptibility of SCID mice to mucosal (tongue and stomach) candidiasis. Gnotobiotic (C. albicans-colonized) SCID mice were also found to be as resistant as immunocompetent BALB/c mice to acute (intravenous challenge) renal candidiasis. Colonization of the alimentary tract with a bacterial flora appeared to enhance the resistance of SCID mice to disseminated candidiasis. This study demonstrates that innate immune mechanisms (phagocytic and/or NK cells), in the absence of functional T- and B-cells, play an important role in the resistance of SCID mice to mucosal and disseminated candidiasis of endogenous (intestinal tract) or acute (intravenous challenge) origin.