Immune aging and infectious diseases.
Abstract
The rise in global life expectancy has led to an increase in the older population, presenting significant challenges in managing infectious diseases. Aging affects the innate and adaptive immune systems, resulting in chronic low-grade inflammation (inflammaging) and immune function decline (immunosenescence). These changes would impair defense mechanisms, increase susceptibility to infections and reduce vaccine efficacy in older adults. Cellular senescence exacerbates these issues by releasing pro-inflammatory factors, further perpetuating chronic inflammation. Moreover, comorbidities, such as cardiovascular disease and diabetes, which are common in older adults, amplify immune dysfunction, while immunosuppressive medications further complicate responses to infections. This review explores the molecular and cellular mechanisms driving inflammaging and immunosenescence, focusing on genomic instability, telomere attrition, and mitochondrial dysfunction. Additionally, we discussed how aging-associated immune alterations influence responses to bacterial, viral, and parasitic infections and evaluated emerging antiaging strategies, aimed at mitigating these effects to improve health outcomes in the aging population.
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Research summary
The paper addresses the mechanisms of immune aging and their implications for infectious diseases, which are critical aspects of longevity research. It explores the underlying biological processes such as inflammaging and immunosenescence that contribute to age-related decline in immune function. However, while it provides solid insights into these mechanisms, the focus remains largely on understanding the problem rather than proposing transformative solutions or interventions aimed at directly extending lifespan or reversing aging processes. Thus, it represents a solid contribution but with limited impact on the field.
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