Researchers raised mice in a
The high level summary is simple to outline, but the picture is a complicated one under the hood. Even given just the three broad categories of (a) immune cells, (b) gut microbes, and © pathogens — a dramatic oversimplification of the real picture — we can still argue about the direction of causation. Does exposure to pathogens cause malfunctions in the immune system, that in turn leads to changes in the gut microbe populations, that in turn feed back to cause further immune issues and other problems in intestinal function? Or are direct effects of pathogens on gut microbes more important? Or are other bodily systems involved in a significant way? There is much work yet to be accomplished in this part of the field. Further, the usual caveats apply here despite promising supporting evidence from other parts of the field: mice are not people, and the interactions with pathogens that are important over a mouse life span are unlikely to be the same as those that are most important over a human life span.
That said, there is a good deal of evidence for the aging of the immune system over a normal human life span to be accelerated by exposure to persistent pathogens like cytomegalovirus. An ever increasing fraction of immune cells are dedicated, uselessly, to this class of invader, while other activities are neglected. The immune system malfunctions in ways that promote ever greater inflammation, but with ever less of the usual benefits in terms of increased beneficial immune activity. Transient inflammation in younger people is useful, a necessary part of the way in which the immune system functions. Chronic inflammation in the old, on the other hand, is essentially a form of damage that contributes to the progression of many