Upon infection with a pathogen, eukaryotic cells can undergo programmed
cell death as an ultimate response. Therefore,
modulation of apoptosis is often a prerequisite to establish a host-pathogen
relationship. Some pathogens kill macrophages
by inducing apoptosis and thus overcome the microbicidal arsenal of the
phagocyte. Apoptotic macrophages, on the other
hand, can elicit an inflammation by secretion of proinflammatory cytokines.
Shigella flexneri, the aetiological agent of
bacillary dysentery, induces apoptosis in macrophages which, in agony,
specifically release mature interleukin-1β (IL-1β).
This cytokine attracts neutrophils (PMN) to the site of infection resulting
in the massive colonic inflammation characteristic of bacillary dysentery.
Shigellosis represents a paradigm of a proinflammatory apoptosis in a bacterial
infection.
The molecular link between apoptosis and inflammation is interleukin-1β
converting enzyme (ICE) which is activated
during macrophage apoptosis and binds to IpaB, a secreted Shigella
protein.