Gois Luana, Badaró Roberto, Schooley Robert, Grassi Maria Fernanda Rios
Centro de Pesquisas Gonçalo Moniz, Fundação Oswaldo Cruz (FIOCRUZ), Salvador, Bahia, Brazil.
Hospital Professor Edgard Santos, Universidade Federal da Bahia, Salvador, Bahia, Brazil.
BMC Infect Dis. 2015 Feb 3;15:38. doi: 10.1186/s12879-015-0774-6.
After the onset of HAART, some HIV-infected individuals under treatment present a exacerbated inflammation in response to a latent or a previously treated opportunistic pathogen termed immune reconstitution inflammatory syndrome (IRIS). Few reports of tegumentary leishmaniasis have been described in association with IRIS. Moreover, the immunopathogenesis of IRIS in association with Leishmania is unclear.
The present study reports on a 29-year-old HIV-infected individual who developed mucocutaneous leishmaniasis associated with immune reconstitution inflammatory syndrome (IRIS) five months following highly active antiretroviral therapy (HAART). Severe lesions resulted in the partial destruction of the nasal septum, with improvement observed 15 days after treatment with Amphotericin B and corticosteroids. The immune response of this patient was evaluated before and after the lesions healed. IRIS was diagnosed in association with high levels of TNF-α and IL-6. Decreased production of IFN-γ and a low IFN-γ/IL-10 ratio were also observed in response to Leishmania antigens. After receiving anti-leishmanial treatment, the individual's specific Th1 immune response was restored.
The results suggest that the production of inflammatory cytokines by unstimulated T-lymphocytes could contribute to occurrence of leishmaniasis associated with IRIS.
高效抗逆转录病毒治疗(HAART)开始后,一些接受治疗的HIV感染者会因潜在的或先前已治疗的机会性病原体而出现炎症加剧,这被称为免疫重建炎症综合征(IRIS)。与IRIS相关的皮肤利什曼病的报道很少。此外,与利什曼原虫相关的IRIS的免疫发病机制尚不清楚。
本研究报告了一名29岁的HIV感染者,在接受高效抗逆转录病毒治疗(HAART)五个月后出现了与免疫重建炎症综合征(IRIS)相关的皮肤黏膜利什曼病。严重病变导致鼻中隔部分破坏,在用两性霉素B和皮质类固醇治疗15天后病情有所改善。在病变愈合前后对该患者的免疫反应进行了评估。诊断为与高水平的肿瘤坏死因子-α和白细胞介素-6相关的IRIS。对利什曼原虫抗原的反应还观察到干扰素-γ产生减少和干扰素-γ/白细胞介素-10比值降低。接受抗利什曼原虫治疗后,该个体的特异性Th1免疫反应得以恢复。
结果表明,未受刺激的T淋巴细胞产生炎症细胞因子可能导致与IRIS相关的利什曼病的发生。