硫化氢在细菌中的代谢和功能以及与结核分枝杆菌的相互作用

Bidirectional interactions of hydrogen sulfide and Mycobacterium tuberculosis

真核细胞和细菌使用相同的底物和酶,但通过不同的反转硫酰化和转硫酰化途径产生硫化氢(H_(2)S)。细菌产生的H_(2)S不仅支持其自身存活,还向宿主传递微生物群稳态的信息。细菌性疾病对人类健康产生诸多负面影响,如加剧肥胖、糖尿病、炎症性肠病和哮喘等疾病的发展。这些病理变化与硫化氢的代谢和功能异常密切相关。宿主产生的H_(2)S因具体情况的不同而发挥保护细菌或杀灭细菌的作用。宿主与细菌通过各自产生的H_(2)S发挥着相互作用,这种相互作用对于与硫化氢相关的结核病病因学尤其具有启示意义。结核病由结核分枝杆菌(MTB)引起,H_(2)S具有促进MTB存活和生长的作用。故而,通过抑制宿主和MTB产生H_(2)S从而达到治疗结核病的目的,将是结核病防治研究的一种新策略。

Eukaryotes and bacteria produce H_(2)S,using the same substrates and enzymes which constitute reverse-trans-sulfuration and trans-sulfuration pathways.Bacterium-made H_(2)S supports their own survival and signals the host of the status of microbiota homeostasis.Bacterial diseases negatively affect human health,exacerbating human diseases like obesity,diabetes,inflammatory bowel diseases,and asthma.By no coincidence,these pathological situations are also tightly related to abnormal metabolism and function of H_(2)S signal.Host-made H_(2)S offers both bacterial protective and bactericidal effects under different circumstances.These bidirectional interactions become especially informative for H_(2)S-related pathogenesis of tuberculosis,caused by Mycobacterium tuberculosis(MTB).As H_(2)S promotes MTB survival and growth,a novel intervention strategy for tuberculosis is called to inhibit the production of both host-derived and MTB-made H_(2)S in order to suppress pathogenesis of tuberculosis.