Kiran Dilara, Podell Brendan K, Chambers Mark, Basaraba Randall J
Department of Microbiology, Immunology and Pathology, Metabolism of Infectious Diseases Laboratory and Mycobacteria Research Laboratories, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, 200 West Lake Street, 1619 Campus Delivery, Fort Collins, CO, 80523-1619, USA.
Department of Bacteriology, Animal and Plant Health Agency (APHA), Woodham Lane, New Haw, Addlestone, Surrey, KT15 3NB, UK.
Semin Immunopathol. 2016 Mar;38(2):167-83. doi: 10.1007/s00281-015-0537-x. Epub 2015 Oct 28.
Infection by the intracellular bacterial pathogen Mycobacterium tuberculosis (Mtb) is a major cause of morbidity and mortality worldwide. Slow progress has been made in lessening the impact of tuberculosis (TB) on human health, especially in parts of the world where Mtb is endemic. Due to the complexity of TB disease, there is still an urgent need to improve diagnosis, prevention, and treatment strategies to control global spread of disease. Active research targeting avenues to prevent infection or transmission through vaccination, to diagnose asymptomatic carriers of Mtb, and to improve antimicrobial drug treatment responses is ongoing. However, this research is hampered by a relatively poor understanding of the pathogenesis of early infection and the factors that contribute to host susceptibility, protection, and the development of active disease. There is increasing interest in the development of adjunctive therapy that will aid the host in responding to Mtb infection appropriately thereby improving the effectiveness of current and future drug treatments. In this review, we summarize what is known about the host response to Mtb infection in humans and animal models and highlight potential therapeutic targets involved in TB granuloma formation and resolution. Strategies designed to shift the balance of TB granuloma formation toward protective rather than destructive processes are discussed based on our current knowledge. These therapeutic strategies are based on the assumption that granuloma formation, although thought to prevent the spread of the tubercle bacillus within and between individuals contributes to manifestations of active TB disease in human patients when left unchecked. This effect of granuloma formation favors the spread of infection and impairs antimicrobial drug treatment. By gaining a better understanding of the mechanisms by which Mtb infection contributes to irreversible tissue damage, down regulates protective immune responses, and delays tissue healing, new treatment strategies can be rationally designed. Granuloma-targeted therapy is advantageous because it allows for the repurpose of existing drugs used to treat other communicable and non-communicable diseases as adjunctive therapies combined with existing and future anti-TB drugs. Thus, the development of adjunctive, granuloma-targeted therapy, like other host-directed therapies, may benefit from the availability of approved drugs to aid in treatment and prevention of TB. In this review, we have attempted to summarize the results of published studies in the context of new innovative approaches to host-directed therapy that need to be more thoroughly explored in pre-clinical animal studies and in human clinical trials.
细胞内细菌病原体结核分枝杆菌(Mtb)感染是全球发病和死亡的主要原因。在减轻结核病(TB)对人类健康的影响方面进展缓慢,尤其是在Mtb流行的世界部分地区。由于结核病的复杂性,仍然迫切需要改进诊断、预防和治疗策略,以控制疾病的全球传播。针对通过疫苗接种预防感染或传播、诊断Mtb无症状携带者以及改善抗菌药物治疗反应的途径的积极研究正在进行中。然而,这项研究受到对早期感染发病机制以及导致宿主易感性、保护作用和活动性疾病发展的因素了解相对不足的阻碍。人们对开发辅助治疗的兴趣日益浓厚,这种辅助治疗将帮助宿主适当地应对Mtb感染,从而提高当前和未来药物治疗的有效性。在这篇综述中,我们总结了关于人类和动物模型中宿主对Mtb感染反应的已知情况,并强调了参与结核肉芽肿形成和消散的潜在治疗靶点。基于我们目前的知识,讨论了旨在将结核肉芽肿形成的平衡转向保护性而非破坏性过程的策略。这些治疗策略基于这样一种假设,即肉芽肿形成虽然被认为可以防止结核杆菌在个体内部和个体之间传播,但如果不加以控制,会导致人类患者出现活动性结核病的表现。肉芽肿形成的这种作用有利于感染的传播并损害抗菌药物治疗。通过更好地理解Mtb感染导致不可逆组织损伤、下调保护性免疫反应以及延迟组织愈合的机制,可以合理设计新的治疗策略。针对肉芽肿的治疗具有优势,因为它允许将用于治疗其他传染病和非传染病的现有药物重新用作辅助治疗,与现有和未来的抗结核药物联合使用。因此,与其他宿主导向疗法一样,开发针对肉芽肿的辅助治疗可能受益于已批准药物的可用性,以帮助治疗和预防结核病。在这篇综述中,我们试图在宿主导向疗法的新创新方法的背景下总结已发表研究的结果,这些方法需要在临床前动物研究和人类临床试验中进行更深入的探索。