Ageing alters the competence of the immune system to control parasitic infection

Abstract

The elderly are more susceptible to infections with various pathogenic organisms than are young-adults or middle-aged individuals. Certain microorganisms that are non-pathogenic in adults may cause serious infections in the elderly. This heightened susceptibility of the elderly is most likely a reflection of the age-associated decline in the competence of the immune system. It appears that the population of T cells is altered with advanced age and, possibly, the efficiency of the monocyte/macrophage cells to destroy microbial invaders declines. There is a small, but compelling, body of literature which shows that the elderly are particularly susceptible to protozoan and metazoan parasites. We have studied the markedly increased severity of infections in aged mice with the mouse-specific Trypanosoma musculi; both the parasite burden and the duration of infection are substantially greater in old compared to young mice. It appears that this difference is due, to a large extent, to the relatively weak ability of aged animals to generate cytokines associated with the TH1 subset of CD4 + T cells; in particular, the weak ability to generate IL-2 and IFNγ which are involved in the selective expression of curative, parasite-specific antibody of the IgG2a isotype. A striking difference between young and aged mice is in the response of IL-3 producing cells to the parasite infection; IL-3-producers decline during infection in young mice but increase markedly in aged animals. There are several advantages to using T. musculi as a prototype pathogen for studying age-related susceptibility to infection. One of the important features of this system is its relevance to a potential major health problem among the elderly; viz., parasitic infections resulting from the rapid extension of human life expectancy and the increasing probability of contact with immunodeficient individuals suffering from opportunistic, parasitic infections.