Facultad de Medicina, Universidad de Antioquia, Medellín, Colombia.
Cell Immunol. 2011;270(2):145-55. doi: 10.1016/j.cellimm.2011.04.009. Epub 2011 Apr 29.
The blockade of sPLA-2, as well as the removal of calcium during the infection with Mycobacterium tuberculosis, prevents necrosis in mononuclear phagocytes. In addition, previous evidence indicates that the necrosis is modulated by cytokines and may condition the inflammatory environment. The production of cytokines and chemokines in response to infection with M. tuberculosis, fatty acid profile and the lactate dehydrogenase activity in mononuclear phagocytes from tuberculosis patients and healthy controls were interrelated using a principal component analysis in order to establish whether there was an association between the induction and effector stages of necrosis with the production of cytokines and chemokines. Differentiation increased the ratio of saturated/unsaturated fatty acids. The oleate and palmitate correlated with differentiation, laureate, arachidonate and linolenate with infection and necrosis correlates with the production of IL-10. Monocytes from tuberculosis patients seem to be lees differentiated ex vivo.
阻断 sPLA-2 以及在感染结核分枝杆菌时去除钙可以防止单核吞噬细胞发生坏死。此外，先前的证据表明坏死受细胞因子调节，并可能影响炎症环境。使用主成分分析来研究结核分枝杆菌感染后单核吞噬细胞中细胞因子和趋化因子的产生、脂肪酸谱以及乳酸脱氢酶活性之间的关系，以确定坏死的诱导和效应阶段与细胞因子和趋化因子的产生之间是否存在关联。分化增加了饱和/不饱和脂肪酸的比例。油酸和棕榈酸与分化相关，月桂酸、花生四烯酸和亚麻酸与感染相关，而与坏死相关的是 IL-10 的产生。来自肺结核患者的单核细胞在体外似乎分化较差。
