Innate immune responses in the ageing lung

Abstract

SummaryThe world is undergoing an unprecedented shift in demographics, with the number of individuals over the age of 60 years projected to reach 2 billion or more by 2050, representing 22% of the global population. Elderly people are at a higher risk for chronic disease and more susceptible to infection, due in part to age-related dysfunction of the immune system resulting from low-grade chronic inflammation known as 'inflamm-ageing'. The innate immune system of older individuals exhibits a diminished ability to respond to microbial threats and clear infections, resulting in a greater occurrence of many infectious diseases in elderly people. In particular, the incidence of and mortality from lung infections increase sharply with age, with such infections often leading to worse outcomes, prolonged hospital stays and life-threatening complications, such as sepsis or acute respiratory distress syndrome. In this review, we highlight research on bacterial pneumonias and pulmonary viral infections and discuss age-related changes in innate immunity that contribute to the higher rate of these infections in older populations. By understanding more clearly the innate immune defects in elderly individuals, we can design age-specific therapies to address lung infections in such a vulnerable population.

Lung ageing and COPD: is there a role for ageing in abnormal tissue repair?

“…The first of these relates to dampened immune responses following an infection or injury and the second relates to chronic activation of immune responses in aged subjects in the absence of a real immunological challenge [12]. As a result of immunosenescence, innate and adaptive immune responses decrease with age, characterised by an increase in memory and effector cells at the expense of naïve T-cells and the overall T-cell repertoire [13,14]. Of interest, several of the pro-inflammatory mediators associated with inflammaging, such as tumour necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, are present as pro-inflammatory mediators in the senescence-associated secretory phenotype.…”

A1 adenosine receptor signaling reducesStreptococcus pneumoniaeadherence to pulmonary epithelial cells by targeting expression of platelet‐activating factor receptor

“…The majority of pneumococcal infections occur in elderly individuals ≥65 years of age (Chong & Street, 2008). As the number of elderly individuals is projected to double in the coming decades, reaching 2 billion by 2050, pneumococcal infections pose a serious health concern and an economic burden which calls for novel interventions to fight this disease (Boe, Boule, & Kovacs, 2017).…”

The diversity of myeloid immune cells shaping wound repair and fibrosis in the lung

“…It is well known that the immune system changes with age and there is evidence that this phenomenon known as “immunosenescence” is contributing to the development of age‐related diseases, including pulmonary fibrosis (Boe et al., ; Chilosi, Carloni, Rossi, & Poletti, ; Frasca & Blomberg, ). One of the best‐known characteristics of an aged immune system is the low‐grade chronic pro‐inflammatory state known as “inflammageing” (Frasca & Blomberg, ).…”