University of Cologne researchers led by Hamid Kashkar explain how certain bacteria can override apoptosis in the current issue of Nature Microbiology. They specifically focused on Shigella bacteria, which use lipopolysaccharides (LPS) on their surface to block the effector caspases.
Various bacterial pathogens can escape our immune system by multiplying intracellularly. The intracellular propagation of pathogens later leads to cell breakdown and the release of microorganisms that infect neighboring cells, spread and cause tissue damage, and infectious disease. However, the body has a response to this bacterial strategy: programmed cell death, or apoptosis, reacts to cellular stress situations during infections and causes quick suicide of the infected cells.
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Scientists have observed in the past that pathogens can effectively block apoptosis, allowing them to reproduce and spread intracellularly. However, the molecular mechanism responsible for how these bacteria 'outsmarted' the immune system was largely unknown.
The Kashkar lab showed that the pathogen that causes shigellosis (Shigella), a typical cause of acute inflammatory diarrhoea, blocks apoptosis by efficiently blocking caspases, which act as engines that initiate apoptosis. The biologists showed that lipopolysaccharides bind and block the caspase. Bacteria without complete LPS, on the other hand, spark apoptosis, which blocks them from reproducing intracellularly, and they are successfully eliminated by the immune system and thus no longer able to cause infectious diseases.