Reyes-Ruvalcaba David, González-Cortés Carolina, Rivero-Lezcano Octavio M
Unit of Investigation, Hospital of León, León, Spain.
Immunol Lett. 2008 Feb 15;116(1):72-8. doi: 10.1016/j.imlet.2007.11.010. Epub 2007 Dec 7.
Non-pathogenic mycobacteria, like Mycobacterium gordonae, are rarely associated to disease. The analysis of the mechanisms which are successful against them in the human host may provide useful information to understand why they fail against the pathogenic M. tuberculosis. We have developed an infection model to test the ability of human phagocytes to kill two strains of M. gordonae, HL184G and an attenuated variety, HL184Gat. As controls we included a strain of M. tuberculosis (HL186T) and another one of L. pneumophila (ATCC13151). We observed that human phagocytes lack the intrinsic ability to eliminate either M. gordonae or M. tuberculosis, but they can kill the attenuated strain. We found a relationship between pathogenicity and the pattern of cytokine production. Thus, both the pathogenic M. tuberculosis and Legionella pneumophila, but not the non-pathogenic M. gordonae, induced the production of significantly different levels of IL-1beta, IL-6 and TNF-alpha in monocytes and IL-8 in neutrophils. Although both monocytes and neutrophils killed HL184Gat, but not HL184G, the patterns of cytokine production induced by either strain were identical. Addition of INF-gamma and/or TNF-alpha did not enhance the antimycobacterial activity of phagocytes.
非致病性分枝杆菌，如戈登分枝杆菌，很少与疾病相关。分析人类宿主中针对它们成功的机制，可能会为理解它们为何对致病性结核分枝杆菌失效提供有用信息。我们建立了一个感染模型，以测试人类吞噬细胞杀死两株戈登分枝杆菌HL184G及其减毒株HL184Gat的能力。作为对照，我们纳入了一株结核分枝杆菌（HL186T）和另一株嗜肺军团菌（ATCC13151）。我们观察到，人类吞噬细胞缺乏消除戈登分枝杆菌或结核分枝杆菌的内在能力，但它们可以杀死减毒株。我们发现致病性与细胞因子产生模式之间存在关联。因此，致病性结核分枝杆菌和嗜肺军团菌，而非非致病性戈登分枝杆菌，在单核细胞中诱导产生的IL-1β、IL-6和TNF-α水平以及在中性粒细胞中诱导产生的IL-8水平存在显著差异。尽管单核细胞和中性粒细胞都能杀死HL184Gat，而不能杀死HL184G，但两种菌株诱导的细胞因子产生模式是相同的。添加INF-γ和/或TNF-α并未增强吞噬细胞的抗分枝杆菌活性。
