Elderly individuals have an increased susceptibility to microbial
infections because of age-related anatomical, physiological, and environmental factors. However, the mechanism of aging-dependent susceptibility to
infection is not fully understood. Here, we found that caveolae-dependent endocytosis is elevated in senescent cells. Thus, we focused on the implications of caveolae-dependent endocytosis using Salmonella typhimurium, which causes a variety of diseases in humans and animals by invading the eukaryotic host cell. Salmonella invasion increased in nonphagocytotic senescent host cells in which
caveolin-1 was also increased. When caveolae structures were disrupted by
methyl-beta-cyclodextrin or
siRNA of
caveolin-1 in the senescent cells, Salmonellae invasion was reduced markedly compared to that in nonsenescent cells. In contrast, the over-expression of
caveolin-1 led to increased Salmonellae invasion in nonsenescent cells. Moreover, in aged mice,
caveolin-1 was found to be highly expressed in Peyer's patch and spleen, which are targets for
infection by Salmonellae. These results suggest that high levels of caveolae and
caveolin-1 in senescent host cells might be related to the increased susceptibility of elderly individuals to microbial
infections.