Unidad Académica de Ciencias Biológicas, Laboratorio de Bioquímica Molecular e Inmunobiologia, Universidad Autónoma de Zacatecas, Av. Preparatoria S/N. Col. Agronómicas, 98066 Zacatecas, ZAC, Mexico.
Catedra-CONACYT, Avenida Insurgentes Sur 1685, Guadalupe Inn, 01020 Álvaro Obregón, CDMX, Mexico.
Biomed Res Int. 2017;2017:8796760. doi: 10.1155/2017/8796760. Epub 2017 Sep 27.
The role of type I IFNs in the pathogenesis and control of mycobacterial infection is still controversial. It has been reported that type I IFNs exacerbated infection through hampering Th1 type cellular immune response. However, under certain conditions they can act as natural immune adjuvants for commercial vaccines. At this point, we have reported recently that successive IFN-alpha boosting of (BCG) vaccinated mice protected adult mice from intradermal infection and a difference in iNOS was observed. In the present work, we have found that intramuscular IFN- boosting of (BCG) vaccine, either in vitro (human cell line or macrophages derived from PBMC) or in vivo (aerosol mouse model of infection), promoted mostly the development of specific anti-antimycobacterial Th1 type cytokines (IFN-; IL-12, TNF-alpha, and IL-17; IL1) while bacterial load reduction (0.9 logs versus PBS or BCG vaccine) was observed. These findings indicate that, under the experimental settings reported here, interferon alpha can drive or affect the TH cellular immune response in favour of BCG-inducing immunity against infection.
I 型干扰素在分枝杆菌感染的发病机制和控制中的作用仍存在争议。据报道，I 型干扰素通过阻碍 Th1 型细胞免疫应答而加重感染。然而，在某些情况下，它们可以作为商业疫苗的天然免疫佐剂。在这一点上，我们最近报道了连续 IFN-α增强卡介苗（BCG）接种小鼠对皮内分枝杆菌感染的保护作用，并观察到 iNOS 的差异。在本工作中，我们发现肌肉内 IFN-增强 BCG 疫苗，无论是在体外（人细胞系或源自 PBMC 的巨噬细胞）还是在体内（分枝杆菌感染的气溶胶小鼠模型），主要促进了针对抗分枝杆菌的 Th1 型细胞因子（IFN-γ；IL-12、TNF-α和 IL-17；IL-1）的特异性产生，而观察到细菌载量减少（与 PBS 或 BCG 疫苗相比减少 0.9 对数）。这些发现表明，在本文报道的实验条件下，干扰素-α可以驱动或影响 TH 细胞免疫应答，有利于 BCG 诱导的针对分枝杆菌感染的免疫。
