Another use for apoptosis

When learning of programmed cell death - apoptosis - many students often rightly question its use. At this point the lecturer will usually trot out a few well-worn examples (like chiseling away tissue from our embryonic hands to make five individual fingers), but it isn't often considered that cell loss is might sometimes be mechanism to prevent infection. (Amongst other theories, this has been postulated as the reason for the gut epithelium's high turnover rate, and even for menstruation.) Here's some research of a less speculative nature that you might find interesting.

Legionella pneumophila is the aerobic Gram-negative bacterium that causes Legionnaire's disease. It does most of its damage as an intracellular parasite within our macrophages. A recent study has shone light on why it is that our dendritic cells aren't as easily affected as our macrophages are.

Dendritic cells are, like macrophages, phagocytes and antigen-presenting cells. They are present in such diverse tissues as the skin, lung, nose and gastrointestinal tract, and they play a major role in the elimination of pathogens.

In many ways, dendritic cells are closely related to macrophages. So why are they resistant to infection by L. pneumophila, while macrophages aren't? The answer appears to be that our dendritic cells are rigged in a particular manner, so that if they become infected by L. pneumophila, they 'autodestruct' - i.e. undergo apoptosis. Needless to say, this "scorched earth" policy severely limits the ability of this pathogen to mount a successful attack on us.

The authors conclude:

"DCs [dendritic cells] are very proficient at migrating from peripheral tissues to the host lymphatic system following exposure to maturation stimuli, such as encounters with microbes. Because of this property, it has been suggested that DCs can function as a “Trojan Horse” capable of systemic dissemination of pathogens internalized at peripheral sites of infection. Here we show that rapid cell death is one mechanism DCs use to avoid being subverted by an intracellular pathogen. In addition to preventing pathogen replication and dissemination, apoptotic DCs harboring intracellular pathogens would become substrates for phagocytosis by neighboring DCs and macrophages, and most mechanisms used by intracellular pathogens to subvert host cellular function would be ineffective as long as the pathogen were residing in an apoptotic cell. Thus, apoptotic bodies containing pathogens would be degraded in lysosomes, resulting in the release of pathogen-derived molecules that could stimulate innate immune receptors and trigger adaptive responses by being presented on the cell surface in association with host MHC proteins. Based on these data, we hypothesize that rapid pathogen-induced apoptosis by DCs is an important innate immune response to intracellular pathogens."