Farah C S, Elahi S, Pang G, Gotjamanos T, Seymour G J, Clancy R L, Ashman R B
Oral Biology and Pathology, School of Dentistry, University of Queensland, Brisbane, Queensland 4072, Australia.
Infect Immun. 2001 Oct;69(10):6110-8. doi: 10.1128/IAI.69.10.6110-6118.2001.
The purpose of this study was to identify the cell populations involved in recovery from oral infections with Candida albicans. Monoclonal antibodies specific for CD4+ cells, CD8+ cells, and polymorphonuclear leukocytes were used to deplete BALB/c and CBA/CaH mice of the relevant cell populations in systemic circulation. Monocytes were inactivated with the cytotoxic chemical carrageenan. Mice were infected with 10(8) C. albicans yeast cells and monitored for 21 days. Systemic depletion of CD4+ and CD8+ T lymphocytes alone did not increase the severity of oral infection compared to that of controls. Oral colonization persisted in animals treated with head and neck irradiation and depleted of CD4+ T cells, whereas infections in animals that received head and neck irradiation alone or irradiation and anti-CD8 antibody cleared the infection in a comparable fashion. The depletion of polymorphonuclear cells and the cytotoxic inactivation of mononuclear phagocytes significantly increased the severity of oral infection in both BALB/c and CBA/CaH mice. High levels of interleukin 12 (IL-12) and gamma interferon (IFN-gamma) were produced by lymphocytes from the draining lymph nodes of recovering animals, whereas IL-6, tumor necrosis factor alpha, and IFN-gamma were detected in the oral mucosae of both naïve and infected mice. The results indicate that recovery from oropharyngeal candidiasis in this model is dependent on CD4+-T-cell augmentation of monocyte and neutrophil functions exerted by Th1-type cytokines such as IL-12 and IFN-gamma.
本研究的目的是确定参与从白色念珠菌口腔感染中恢复的细胞群体。使用针对CD4 +细胞、CD8 +细胞和多形核白细胞的单克隆抗体，使BALB/c和CBA/CaH小鼠全身循环中的相关细胞群体减少。单核细胞用细胞毒性化学物质角叉菜胶使其失活。小鼠感染10(8)个白色念珠菌酵母细胞，并监测21天。与对照组相比，单独全身消耗CD4 +和CD8 + T淋巴细胞并没有增加口腔感染的严重程度。接受头颈部照射并消耗CD4 + T细胞的动物口腔定植持续存在，而仅接受头颈部照射或照射和抗CD8抗体的动物感染以类似方式清除。多形核细胞的消耗和单核吞噬细胞的细胞毒性失活显著增加了BALB/c和CBA/CaH小鼠口腔感染的严重程度。恢复动物引流淋巴结中的淋巴细胞产生高水平的白细胞介素12（IL-12）和γ干扰素（IFN-γ），而在未感染和感染小鼠的口腔黏膜中均检测到IL-6、肿瘤坏死因子α和IFN-γ。结果表明，在该模型中从口咽念珠菌病中恢复取决于CD4 + T细胞增强单核细胞和中性粒细胞的功能，这是由Th1型细胞因子如IL-12和IFN-γ发挥作用的。
