Recent forecasts estimate that the proportion of individuals aged >60 years, who accounted for 10 % of the global population in the year 2000, will constitute 21 % of the world’s population by 2050 [1]. A testament to advancements in medical care and public health policies, an increase in life expectancy should be viewed favourably. However, with ageing defined as “the increasing frailty of an organism with time that reduces their ability to deal with stress, resulting in an increased chance of disease” [2], an extension in life expectancy does not necessarily mean these “additional years” will be experienced in good health.

Infectious diseases are a common occurrence amongst older people, with this section of society reporting increased episodes of urinary tract infections [3], influenza [4] and community-acquired pneumonia [5] when compared to their younger counterparts. In addition, infection severity is greater, with older adults reporting significantly increased infection-related morbidity and mortality rates [6, 7]. Thought to underlie this increased incidence and severity of infection are age- associated changes in immune function, a phenomenon termed immunosenescence. Whilst it has been known for many years that ageing has a profound effect upon adaptive immunity [8], only recently has it become evident that the innate arm of the immune system undergoes considerable age-related re-modelling. For instance, alongside alterations in the efficiency of innate barriers and the composition of the humoral arm of innate immunity [9,10], significant differences exist in the composition, phenotype and function of the cellular arm of innate immunity between young and older adults. In this chapter, we provide a detailed overview of the impact that age has on four cell types central to the innate immune response; neutrophils, natural killer (NK) cells, dendritic cells (DCs) and monocytes/macrophages. Furthermore, with it now recognised that the function of the innate immune system extends beyond the recognition and elimination of pathogens [11-14], we discuss how innate immunosenescence may have more far reaching consequences for the health of older adults than simply increasing their susceptibility to infection.

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