Nandi Ajeya, Bishayi Biswadev
Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, APC Road, Calcutta 700009, West Bengal, India.
Department of Physiology, Immunology Laboratory, University of Calcutta, University Colleges of Science and Technology, APC Road, Calcutta 700009, West Bengal, India.
Microb Pathog. 2015 Dec;89:114-27. doi: 10.1016/j.micpath.2015.09.007. Epub 2015 Sep 28.
Staphylococcus aureus is an important pathogen in bone disease and innate immune recognition receptor, TLR-2 is reported to be crucial for inflammatory bone loss. Role of TLR-2 in bacterial clearance and cytokine response to S. aureus infection in murine bone marrow macrophages has been reported but the role of host derived ROS in host-pathogen relationship still remains an obvious question. In the present study, blocking of SOD and catalase in TLR-2 neutralized fresh bone marrow cells (FBMC) with Diethyldithiocarbamic acid (DDC) and 3-Amino-1,2,4-triazole (ATZ), separately, during acute S. aureus infection, produces moderate level of ROS and limits inflammation as compared with only TLR-2 non-neutralized condition and leads to decreased bacterial count compared with only TLR-2 neutralized condition. In summary, host SOD and catalase modulates ROS generation, cytokine levels and TLR-2 expression in FBMCs during acute S. aureus infection which might be useful in the alleviation of S. aureus infection and bone loss.
金黄色葡萄球菌是骨病中的一种重要病原体，据报道，天然免疫识别受体TLR-2对炎症性骨质流失至关重要。TLR-2在小鼠骨髓巨噬细胞中对金黄色葡萄球菌感染的细菌清除和细胞因子反应中的作用已有报道，但宿主来源的活性氧在宿主-病原体关系中的作用仍然是一个明显的问题。在本研究中，在急性金黄色葡萄球菌感染期间，分别用二乙基二硫代氨基甲酸（DDC）和3-氨基-1,2,4-三唑（ATZ）阻断TLR-2中和的新鲜骨髓细胞（FBMC）中的超氧化物歧化酶（SOD）和过氧化氢酶，与仅TLR-2未中和的情况相比，产生中等水平的活性氧并限制炎症，与仅TLR-2中和的情况相比导致细菌数量减少。总之，在急性金黄色葡萄球菌感染期间，宿主SOD和过氧化氢酶调节FBMC中活性氧的产生、细胞因子水平和TLR-2表达，这可能有助于减轻金黄色葡萄球菌感染和骨质流失。
