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A Decline in p38 MAPK Signaling Underlies Immunosenescence in Caenorhabditis elegans

Figure 6

A cycle of intestinal tissue aging, immunosenescence, and progressive intestinal proliferation of bacteria towards the end of life in C. elegans.

(A) Fraction of wild type N2 C. elegans (white bars) or pmk-1(km25) mutants (grey bars) maintained on lawns of E. coli OP50 that exhibit intestinal distention at Days 6, 9, and 12 of adulthood. Inset, ratio of the average number of pmk-1 mutants with intestinal distention versus the average number of wild type animals with intestinal distention at Days 6, 9, or 12 of adulthood. (B) As the primary immune cells in C. elegans, age-related damage to intestinal cells may impair their ability to execute processes required for immune protection, such as the expression of immune effector proteins, including those regulated by the PMK-1 pathway. The consequent reduction in host defense would lead to increased colonization of the C. elegans intestine by pathogenic microbes, which contribute to and amplify intestinal cell deterioration during the infection process. Thus a self-perpetuating cycle of increased intestinal deterioration, decreased immunity, and increased accumulation of bacteria may underlie immunosenescence and significantly contribute to mortality later in life.

Figure 6