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Am J Respir Crit Care Med :强力霉素或可治疗肺结核

  1. 强力霉素
  2. 肺结核

来源:中国科技网 2012-11-18 10:54

近日,英国帝国理工学院等机构研究人员在新一期《美国呼吸道与危重护理学杂志》(American Journal of Respiratory and Critical Care Medicine)上报告了最新发现,已作为抗生素使用多年的药物强力霉素也许还可以用于治疗肺结核,由于这种药物成本低廉,这项发现也许对广大发展中国家的肺结核防治工作来说是个好消息。

近日,英国帝国理工学院等机构研究人员在新一期《美国呼吸道与危重护理学杂志》(American Journal of Respiratory and Critical Care Medicine)上报告了最新发现,已作为抗生素使用多年的药物强力霉素也许还可以用于治疗肺结核,由于这种药物成本低廉,这项发现也许对广大发展中国家的肺结核防治工作来说是个好消息。

据介绍,过去的研究曾发现在肺结核的发病过程中,结核杆菌会使受感染的细胞中生成一种名为MMP-1的酶,这种酶会起到破坏肺部组织的作用。本次研究又发现,强力霉素能抑制生成这种酶的过程,从而帮助治疗肺结核。

研究人员用试管中培养的人类细胞进行了试验,结果显示在强力霉素的作用下,人类细胞虽然被结核杆菌感染,但生成该种酶的数量下降。此外研究人员还进行了动物实验,结果也显示强力霉素可以抑制结核杆菌在实验鼠体内的生长。

领导研究的保罗·埃尔金顿说,对肺结核的疗法在近30年来没有什么大变化,但有抗药性的结核杆菌却不断出现,因此寻找新的治疗药物非常重要。强力霉素虽然已面世数十年,但令人惊讶的是此前一直没有发现它在治疗肺结核方面的效果。为进一步验证这种效果,研究人员接下来将开展人类临床试验。(生物谷Bioon.com)

Doxycycline and HIV Infection Suppress Tuberculosis-induced Matrix Metalloproteinases

Naomi F Walker, Simon O Clark, Tolu On, Nuria Andreu, Liku Tezera, Shivani Singh, Luísa Saraiva, Bernadette Pedersen, Dominic L Kelly, Julia A Tree, Jeanine M D'Armiento11, Graeme Meintjes, Francesco A Mauri, Ann Williams, Robert J Wilkinson, Jon S Friedland and Paul T Elkington

Rationale: Tuberculosis kills over 1.5 million people per year and standard treatment has remained unchanged for over 30 years. Tuberculosis drives matrix metalloproteinase (MMP) activity to cause immunopathology. In advanced HIV infection, tissue destruction is reduced but underlying mechanisms are poorly defined and no current anti-tuberculous therapy reduces host tissue damage. Objectives: To investigate MMP activity in tuberculosis patients with and without HIV co-infection and to determine the potential of doxycycline to inhibit MMPs and decrease pathology. Methods: Concentrations of MMPs and cytokines were analyzed by Luminex array in a prospectively recruited cohort of patients. Modulation of MMP secretion and Mycobacterium tuberculosis growth by doxycycline was studied in primary human cells and tuberculosis-infected guinea pigs. Main Results: HIV co-infection decreased MMP concentrations in induced sputum of tuberculosis patients. MMPs correlated with clinical markers of tissue damage, further implicating dysregulated protease activity in tuberculosis-driven pathology. In contrast, cytokine concentrations were no different. Doxycycline, a licensed MMP inhibitor, suppressed tuberculosis-dependent MMP-1 and -9 secretion from primary human macrophages and epithelial cells by inhibiting promoter activation. In the guinea pig model, doxycycline reduced lung tuberculosis colony forming units after eight weeks in a dose-dependent manner compared to untreated animals, and in vitro doxycycline inhibited mycobacterial proliferation. Conclusions: HIV co-infection in tuberculosis patients reduces concentrations of immunopathogenic MMPs. Doxycycline decreases MMP activity in a cellular model and suppresses mycobacterial growth in vitro and in guinea pigs. Adjunctive doxycycline therapy may reduce morbidity and mortality in tuberculosis.

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