How Mycobacterium tuberculosis ― which causes tuberculosis ― regulates host cell death during infection greatly alters immune cell responses, according to a report published online in Nature Immunology.
Cells can die through two distinct processes. Apoptosis preserves membrane integrity of the cell, while in necrosis the cellular membrane is broken and its content can reach surrounding cells. Pathogens manipulate these cellular death pathways to ensure their survival and propagation. M. tuberculosis, one of the most efficient human pathogens, is known to inhibit apoptosis and promote necrosis of its host cells ― the lung macrophages; necrosis allows the bacteria to spread to healthy neighboring cells.
Samuel Behar and colleagues show that apoptosis is beneficial for the host not just by containing pathogens, but also because vesicles derived from apoptotic cells can enhance the activation of T cells, the main immune system apparatus that fight M. tuberculosis infections. Thus, by inhibiting host cell apoptosis, virulent strains of M. tuberculosis enhance pathogen spread and delay the recruitment of specialized killer cells to the site of infection, with direct consequences in controlling bacterial burden in the lung.
Ecology: Stress-resistant corals maintain heat tolerance under cooler temperaturesNature Communications
Zoology: New electric eel species produces quite a shockNature Communications
Evolution: A virtual skull of modern humans’ last common ancestorNature Communications