Dipartimento di Scienze e Tecnologie Biologiche ed Ambientali, Università del Salento, Via Provinciale Monteroni, 73100 Lecce, Italy.
Mol Microbiol. 2011 Sep;81(5):1330-42. doi: 10.1111/j.1365-2958.2011.07766.x. Epub 2011 Jul 20.
Polymorphonuclear neutrophil leucocytes (PMNs) are a critical part of innate immune defence against bacterial pathogens, and only a limited subset of microbes can escape killing by these phagocytic cells. Here we show that Neisseria meningitidis, a leading cause of septicaemia and meningitis, can avoid killing by PMNs and this is dependent on the ability of the bacterium to acquire L-glutamate through its GltT uptake system. We demonstrate that the uptake of available L-glutamate promotes N. meningitidis evasion of PMN reactive oxygen species produced by the oxidative burst. In the meningococcus, L-glutamate is converted to glutathione, a key molecule for maintaining intracellular redox potential, which protects the bacterium from reactive oxygen species such as hydrogen peroxide. We show that this mechanism contributes to the ability of N. meningitidis to cause bacteraemia, a critical step in the disease process during infections caused by this important human pathogen.
多形核中性粒细胞（PMN）是先天免疫防御细菌病原体的关键部分，只有有限的微生物亚群能够逃避这些吞噬细胞的杀伤。在这里，我们表明，脑膜炎奈瑟菌是败血症和脑膜炎的主要原因，它可以避免被 PMN 杀死，这依赖于细菌通过其 GltT 摄取系统获取 L-谷氨酸的能力。我们证明，可用 L-谷氨酸的摄取促进了脑膜炎奈瑟菌逃避 PMN 氧化爆发产生的活性氧。在脑膜炎奈瑟菌中，L-谷氨酸被转化为谷胱甘肽，这是维持细胞内氧化还原电势的关键分子，它保护细菌免受活性氧（如过氧化氢）的侵害。我们表明，这种机制有助于脑膜炎奈瑟菌引起菌血症的能力，菌血症是由这种重要的人类病原体引起的感染过程中的一个关键步骤。
