Núñez María J, Novío Silvia, Suárez Juan Antonio, Balboa José, Freire-Garabal Manuel
Neuroimmunology Laboratory, Department of Pharmacology, School of Medicine, San Francisco, 15782 Santiago de Compostela, A Coruña, Spain.
Clin Vaccine Immunol. 2010 Apr;17(4):668-73. doi: 10.1128/CVI.00380-09. Epub 2010 Feb 3.
Psychological stress has been found to suppress cell-mediated immune responses that are important for limiting the proliferation of Candida albicans. Fluoxetine has been observed to reduce negative consequences of stress on the immune system in experimental and clinical models, but there are no data on its effects on oral candidiasis. We designed experiments to evaluate the effects of fluoxetine on the development of oral candidiasis in Sprague-Dawley rats exposed to a chronic auditory stressor. Animals were submitted to surgical hyposalivation in order to facilitate the establishment and persistence of C. albicans infection. Stress application and treatment with drugs (placebo or fluoxetine) were initiated 7 days before C. albicans inoculation and lasted until the end of the experiments, on day 15 postinoculation. Establishment of C. albicans infection was evaluated on days 2 and 15 after inoculation. Tissue injury was determined by the quantification of the number and type (normal or abnormal) of papillae on the dorsal tongue per microscopic field. A semiquantitative scale was devised to assess the degree of colonization of the epithelium by fungal hyphae. Our results showed that stress exacerbates C. albicans infection in the tongues of rats. Significant increases in Candida counts, the percentage of the tongue's surface covered with clinical lesions, the percentage of abnormal papillae, and the colonization of the epithelium by hyphae were found in stressed rats compared to the nonstressed ones. Treatment with fluoxetine significantly reversed these adverse effects of stress. Besides the psychopharmacological properties of fluoxetine against stress, it has consequences for Candida infection.
研究发现,心理应激会抑制细胞介导的免疫反应,而这种免疫反应对于限制白色念珠菌的增殖非常重要。在实验模型和临床模型中,已观察到氟西汀可减轻应激对免疫系统的负面影响,但尚无关于其对口腔念珠菌病影响的数据。我们设计了实验,以评估氟西汀对暴露于慢性听觉应激源的Sprague-Dawley大鼠口腔念珠菌病发展的影响。为便于白色念珠菌感染的建立和持续存在,对动物进行了手术致唾液分泌减少。在白色念珠菌接种前7天开始施加应激并给予药物治疗(安慰剂或氟西汀),持续至实验结束,即接种后第15天。在接种后第2天和第15天评估白色念珠菌感染的建立情况。通过对每个显微镜视野下舌背乳头的数量和类型(正常或异常)进行量化来确定组织损伤。设计了一个半定量量表来评估真菌菌丝在上皮中的定植程度。我们的结果表明,应激会加剧大鼠舌头的白色念珠菌感染。与非应激大鼠相比,应激大鼠的念珠菌计数、舌表面出现临床病变的百分比、异常乳头的百分比以及菌丝在上皮中的定植均显著增加。氟西汀治疗显著逆转了应激的这些不利影响。除了氟西汀对抗应激的心理药理学特性外,它对念珠菌感染也有影响。