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How can tuberculosis cause chronic inflammation?

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Pathways of complement activation — inflammation The main function of complement proteins is to aid in the destruction of pathogens by piercing their outer membranes (cell lysis) or by making them more attractive to phagocytic cells such as macrophages (a process known as opsonization). Some complement components also promote inflammation by stimulating cells to release histamine and by attracting phagocytic cells to the site of infection.

Tuberculosis causes chronic inflammation primarily because the causative agent, Mycobacterium tuberculosis, is highly resistant to host immune defenses. The bacterium possesses a thick, waxy cell wall that allows it to survive inside immune cells and persist within tissues for extended periods, preventing the body from eliminating the infection.12

This persistence triggers a specific form of chronic response known as granulomatous inflammation. In this process, the immune system attempts to wall off the pathogen by forming granulomas, which are small collections of modified macrophages called epithelioid cells, typically surrounded by lymphocytes. In the context of tuberculosis, these specific granulomas are referred to as tubercles.1

Because the body cannot easily clear the bacteria, these immune cells remain at the site of infection, leading to ongoing tissue damage and functional impairment characteristic of chronic inflammatory disease.13