Tuberculosis is an important health problem worldwide. The only available vaccine is M. bovis/BCG, an attenuated mycobacterium that activates the innate and the acquired immune system after being phagocytosed by macrophages and dendritic cells. Vaccination fails to prevent adult pulmonary tuberculosis although it may have a protective effect in childhood infection. Understanding how BCG interacts with macrophages and other immunocompetent cells is crucial to develop new vaccines. In this study we showed that macrophages phagocytose M. bovis/BCG bacilli with higher efficiency when they are cultured without phosphate. We isolated mycobacterial membranes to search for mycobacterial molecules that could be involved in these processes; by immunoblot, it was found that the plasma membranes of phosphate-deprived bacilli express the adhesins PstS-1, LpqH, LprG, and the APA antigen. These proteins are not detected in membranes of bacilli grown with usual amounts of phosphate. The interest of our observations is to show that under the metabolic stress implied in phosphate deprivation, mycobacteria respond upregulating adhesins that could improve their capacity to infect macrophages. These observations are relevant to understand how M. bovis/BCG induces protective immunity.

中文翻译：

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磷酸盐饥饿会增强巨噬细胞对牛分枝杆菌/ BCG的吞噬作用。

结核病是世界范围内的重要健康问题。唯一可用的疫苗是牛分枝杆菌/ BCG，这是一种减毒分枝杆菌，在被巨噬细胞和树突状细胞吞噬后会激活先天免疫和后天免疫系统。疫苗接种不能预防成人肺结核，尽管可能对儿童感染有保护作用。了解BCG如何与巨噬细胞和其他具有免疫功能的细胞相互作用是开发新疫苗的关键。在这项研究中，我们显示了巨噬细胞在无磷酸盐的情况下吞噬吞噬牛分枝杆菌/ BCG细菌的效率更高。我们分离了分枝杆菌膜以寻找可能与这些过程有关的分枝杆菌分子。通过免疫印迹发现，磷酸根少的细菌的质膜表达粘附素PstS-1，LpqH，LprG和APA抗原。在用通常量的磷酸盐生长的细菌膜中未检测到这些蛋白质。我们的观察结果的兴趣在于表明，在磷酸盐缺乏所隐含的新陈代谢压力下，分枝杆菌会上调粘附素，从而提高其感染巨噬细胞的能力。这些观察结果与了解牛分枝杆菌/ BCG如何诱导保护性免疫有关。