Department of Immunology, Faculty of Medicine and University Hospital, University Autonomous of Nuevo Leon (UANL), Gonzalitos 235 Norte, Mitras Centro, Monterrey, Nuevo Leon, Mexico.
Department of Histology, Faculty of Medicine, University Autonomous of Nuevo Leon (UANL), Monterrey, Nuevo Leon, Mexico.
Mycopathologia. 2018 Aug;183(4):709-716. doi: 10.1007/s11046-018-0264-7. Epub 2018 May 7.
Coccidioidomycosis is a fungal disease caused by Coccidioides immitis or Coccidioides posadasii. These fungi are endemic in the southern USA and northern Mexico. Immunocompromised patients are susceptible to develop severe forms of this fungal infection. Cytokines play an important role in controlling the fungal infection, but little is known about the predominant immunological environment in human lung tissue from fatal cases. Our aim was to analyze the pro-inflammatory and anti-inflammatory cytokines and monocyte/macrophages markers (CD14 and CD206) in the granulomas of six fatal cases of coccidioidomycosis. Cytokines and surface markers were higher in coccidioidomycosis cases when compared to control (P < 0.05). CD14 positive cells were increased inside the coccidioidal granuloma when compared to the outside (P < 0.05). No differences were found in the number of CD206+ cells inside the granuloma when compared to the outer population (P > 0.05). Interestingly, an analysis of stain intensity signals showed an increased signaling of CD14, CD206, IL-10 and TNFα inside the granuloma when compared to the outside (P < 0.05). iNOS and IL-12 gene expression were not detected in coccidioidomycosis cases, while IL-10, IL-6 and TGFβ gene expression were detected, but the differences when compared to healthy lungs were not significant (P > 0.05). TNFα gene expression was lower in coccidioidomycosis cases when compared to healthy lung (P = 0.05). In conclusion, pro- and anti-inflammatory responses co-exist inside of the granulomas of fatal cases of coccidioidomycosis and the absent of iNOS and IL-12 gene expression may be related with patient's outcome.
球孢子菌病是由粗球孢子菌或波氏球孢子菌引起的真菌病。这些真菌在美国南部和墨西哥北部流行。免疫功能低下的患者易患这种真菌感染的严重形式。细胞因子在控制真菌感染中起着重要作用,但对于致命性球孢子菌病患者肺组织中的主要免疫环境知之甚少。我们的目的是分析 6 例致命性球孢子菌病患者的肉芽肿中的促炎和抗炎细胞因子以及单核细胞/巨噬细胞标志物(CD14 和 CD206)。与对照组相比,球孢子菌病病例中的细胞因子和表面标志物更高(P<0.05)。与外部相比,在球孢子菌肉芽肿内的 CD14 阳性细胞增加(P<0.05)。与外部人群相比,在肉芽肿内的 CD206+细胞数量没有差异(P>0.05)。有趣的是,染色强度信号分析显示,与外部相比,肉芽肿内的 CD14、CD206、IL-10 和 TNFα 的信号强度增加(P<0.05)。在球孢子菌病病例中未检测到 iNOS 和 IL-12 基因表达,而检测到 IL-10、IL-6 和 TGFβ 基因表达,但与健康肺组织相比差异无统计学意义(P>0.05)。与健康肺组织相比,球孢子菌病病例中的 TNFα 基因表达较低(P=0.05)。总之,在致命性球孢子菌病患者的肉芽肿内存在促炎和抗炎反应,而 iNOS 和 IL-12 基因表达缺失可能与患者的结局有关。