Carlos I Z, Zini M M, Sgarbi D B, Angluster J, Alviano C S, Silva C L
Department of Parasitology, Microbiology and Immunology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
Mycopathologia. 1994 Sep;127(3):189-94. doi: 10.1007/BF01102920.
Production of Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF) by adherent peritoneal cells from BALB/c mice was measured at week 2, 4, 6, 8 and 10 after intravenous inoculation with 10(6) Sporothrix schenckii yeasts. As compared with age-matched controls, IL-1 and TNF production by adherent peritoneal cells from S. schenckii-infected mice was reduced severely at week 4 and 6 of infection and greater than normal at week 8 and 10. Moreover, between week 4 and 6 of infection there was a depression of delayed type hypersensitivity response to a specific whole soluble antigen, and an increase in fungal multiplication in the livers and spleens of infected mice. Thus, the deficits of cell-mediated immunity in mice with systemic S. schenckii infection may derive, in part, from impaired amplification of the immune response consequent to abnormal generation of IL-1 and TNF.
在静脉接种10(6) 申克孢子丝菌酵母后第2、4、6、8和10周,检测BALB/c小鼠贴壁腹膜细胞白细胞介素-1(IL-1)和肿瘤坏死因子(TNF)的产生。与年龄匹配的对照相比,感染申克孢子丝菌小鼠的贴壁腹膜细胞产生IL-1和TNF的能力在感染第4周和第6周时严重降低,而在第8周和第10周时高于正常水平。此外,在感染第4周和第6周之间,对特定全可溶性抗原的迟发型超敏反应受到抑制,感染小鼠肝脏和脾脏中的真菌繁殖增加。因此,全身性申克孢子丝菌感染小鼠的细胞介导免疫缺陷可能部分源于IL-1和TNF异常产生导致的免疫反应放大受损。