Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC, USA.
Curr Opin Pharmacol. 2013 Aug;13(4):641-5. doi: 10.1016/j.coph.2013.06.007. Epub 2013 Jul 9.
There is a growing appreciation of the diverse roles that lipid mediators play in modulating inflammatory responses during infection. In the case of tuberculosis, virulent mycobacteria induce host production of anti-inflammatory mediators, including lipoxins, which limit the host inflammatory response and lead to necrotic cell death of infected macrophages. Recent work using the zebrafish model suggests that, while excess anti-inflammatory lipoxins are host detrimental during mycobacterial infections, excess pro-inflammatory lipids also drive host susceptibility. The balance of these inflammatory states is influenced by common human genetic variation in Asia. Fuller understanding of the mechanisms of eicosanoid-mediated inflammatory imbalance during tuberculosis infection has important implications for the development of adjunctive therapies.
人们越来越认识到脂质介质在调节感染期间炎症反应方面的多种作用。就结核病而言，毒力结核分枝杆菌诱导宿主产生抗炎介质，包括脂氧素，它限制宿主炎症反应并导致感染的巨噬细胞发生坏死性细胞死亡。最近使用斑马鱼模型的研究表明，虽然在分枝杆菌感染期间，过量的抗炎性脂氧素对宿主有害，但过量的促炎性脂质也会导致宿主易感性。这些炎症状态的平衡受到亚洲常见的人类遗传变异的影响。充分了解分枝杆菌感染期间类二十烷酸介导的炎症失衡的机制对辅助治疗的发展具有重要意义。
