Figure 1.

The infection pathways of Mycobacterium tuberculosis in human macrophage cells leading to the formation of a granuloma (1-4). Resident alveolar macrophages phagocytes inhaled M. tuberculosis and products the pro-inflammatory response and recruitment of fibroblasts, lymphocytes, neutrophils, natural killer (NK) cells, collagens, necrotic tissues, dendritic cells, foamy macrophages, infected apoptotic macrophage, infected apoptotic epithelial macrophages, and epithelial macrophages, and the formation of a granuloma. However, if the human immune system for any reason is weakened, M. tuberculosis is activated and replicated within the granuloma structure. In this case, the necrotic nucleus of granuloma develops. When the number of M. tuberculosis is increased within the granuloma, it ruptures, and M. tuberculosis is spilled into the airways. Each of the bacteria has the potential to infect other alveolar macrophages to the formation of a new granuloma.