Early life infection and host senescence.

Advanced age is often associated with a chronic inflammatory status and inflammatory diseases. It has been suggested that exposure to infectious agents that stimulate the inflammatory response at early ages might have carry over effects in terms of accelerated senescence and increased mortality at late ages. However, not all pathogens and parasites have pro-inflammatory effects. In particular, parasitic nematodes have been shown to dampen the inflammatory response and to prevent or alleviate the symptoms of inflammatory diseases. We, therefore, tentatively predicted that early infection with a parasite that has anti-inflammatory properties might postpone aging. We tested this idea using the association between the nematode Heligmosomoides polygyrus and its rodent host. In addition to the infection with H. polygyrus, we also activated the systemic inflammatory response with an Escherichia coli LPS injection, to explore the effect of H. polygyrus under control and inflammatory conditions. In addition to lifespan, we also assessed several biomarkers of aging, once the infection had been cleared. We found that both treatments (H. polygyrus infection and LPS challenge) reduced longevity. Most of the biomarkers of aging were affected by the previous infection status, suggesting that mice exposed to the nematode had an accentuated senescent phenotype. These results show that infection with immunomodulatory parasites per se does not prolong host lifespan and rather support the view that infection in early life accelerates the rate of aging.
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