Mycobacterium tuberculosis is able to decide on how best to kill the host cells, thanks to which it minimizes and delays the immune system response of the infected organism, according to scientists from the USA in the pages of the journal Nature Immunology.
Cells can die in at least two main ways. Apoptosis is the process of self-destruction of a cell without compromising the integrity of the cell membrane, while during necrosis, the cell membrane is broken and the contents of the dead cell leak out, affecting neighboring cells.
Some pathogens are able to manipulate the mechanisms of cell death, enabling them to survive and multiply. Mycobacterium tuberculosis is one of the most effective human pathogens. Its strategy is to inhibit apoptosis and increase necrosis of affected macrophages in the lungs, as the necrosis allows bacteria to spread to surrounding healthy cells.
Samuel Behar and colleagues from Brigham and Women’s Hospital and Harvard Medical School in Boston showed that apoptosis is better for an infected organism not only because it limits the spread of mycobacterium, but also because vesicles formed from cells that die by apoptosis activate T cells. and thus help to fight infection.
In turn, inhibition of host cell apoptosis increases the spread of mycobacteria and delays the influx of specialized cells of the immune system, the so-called killer cells to the site of infection, allowing bacteria to occupy the lungs more quickly. (PAP)