Carreto-Binaghi Laura E, Tenorio Eda P, Morales-Villarreal Fernando R, Aliouat El Moukhtar, Zenteno Edgar, Martínez-Orozco José-Arturo, Taylor Maria-Lucia
Laboratorio de Inmunología de Hongos, Unidad de Micología, Departamento de Microbiología-Parasitología, Facultad de Medicina, Universidad Nacional Autónoma de México (UNAM), Mexico City 04510, Mexico.
Laboratorio de Inmunobiología de la Tuberculosis, Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas (INER), Mexico City 14080, Mexico.
J Fungi (Basel). 2021 Nov 4;7(11):938. doi: 10.3390/jof7110938.
Histoplasmosis and pneumocystosis co-infections have been reported mainly in immunocompromised humans and in wild animals. The immunological response to each fungal infection has been described primarily using animal models; however, the host response to concomitant infection is unknown. The present work aimed to evaluate the pulmonary immunological response of patients with pneumonia caused either by , , or their co-infection. We analyzed the pulmonary collectin and cytokine patterns of 131 bronchoalveolar lavage samples, which included HIV and non-HIV patients infected with , , or both fungi, as well as healthy volunteers and HIV patients without the studied fungal infections. Our results showed an increased production of the surfactant protein-A (SP-A) in non-HIV patients with infection, contrasting with HIV patients ( < 0.05). Significant differences in median values of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, IL-33, IL-13, and CXCL8 were found among all the groups studied, suggesting that these cytokines play a role in the local inflammatory processes of histoplasmosis and pneumocystosis. Interestingly, non-HIV patients with co-infection and pneumocystosis alone showed lower levels of SP-A, IL-1β, TNF-α, IFN-γ, IL-18, IL-17A, and IL-23 than histoplasmosis patients, suggesting an immunomodulatory ability of over response.
组织胞浆菌病与肺孢子菌病合并感染主要见于免疫功能低下的人类和野生动物。对每种真菌感染的免疫反应主要是通过动物模型来描述的;然而,宿主对合并感染的反应尚不清楚。本研究旨在评估由、或其合并感染引起的肺炎患者的肺部免疫反应。我们分析了131份支气管肺泡灌洗样本中的肺凝集素和细胞因子模式,这些样本包括感染了、或两种真菌的HIV和非HIV患者,以及健康志愿者和未感染所研究真菌的HIV患者。我们的结果显示,感染的非HIV患者中表面活性蛋白A(SP-A)的产生增加,这与HIV患者形成对比(<0.05)。在所有研究组中,SP-A、IL-1β、TNF-α、IFN-γ、IL-18、IL-17A、IL-33、IL-13和CXCL8的中位数存在显著差异,表明这些细胞因子在组织胞浆菌病和肺孢子菌病的局部炎症过程中起作用。有趣的是,合并感染和单独感染肺孢子菌病的非HIV患者的SP-A、IL-1β、TNF-α、IFN-γ、IL-18、IL-17A和IL-23水平低于组织胞浆菌病患者,这表明对反应具有免疫调节能力。