With advancing age, the human body encounters variousdynamic adjustments. Immunosenescene, a term used to describe age-relatedimpairments in the immune system, is featured as an imbalance between inflammatoryand non-inflammatory mediators. This imbalance will dysregulate adaptive immunityand activate low-grade inflammatory state and make the body more vulnerable toautoimmune diseases 1. These changes are caused by the loss ofability of hematopoietic stem cells (HSCs) to produce lymphoid progenitors and incontrary shifting toward myeloid progenitors. Not only this, but also dysfunctionin monocytes, macrophages, neutrophils and dendritic cells is noted. As aresult, levels of naïve T and B cells as well as T-cell receptor (TCR) andB-cell receptor (BCR) will be significantly decreased. To emphasize more onmacrophages, blood monocyte from aged subjects showed substantial decrease inlevels of TNF-a and IL-6 production, impaired phagocytosis, reduced chemotaxis,and reduce MHC class 2 expression 1.
Aging in particular can mimicmacrophage polarization in the presence of inflammatory factors which shift thepolarization from M2 to M1. Nevertheless, macrophages in adipose tissue of leansubjects mainly express M2 phenotype, in contrast, obese subjects showed higherlevels on M1 phenotype and higher levels of CD4+ and CD8+ T cells as well 1. Another study compared macrophage polarization of splenocytes in youngand aged mice after LPS stimulation, IFNg, TNF-a, and IL-4. After stimulation, noticeablereduction in levels of IL-6, an M1 phenotype mediator from aged mice was noted.Moreover, levels of TNFa, IL-1B, iNOS were markedly reduced in aged micecompared to young mice 2. Certainly, chronic inflammation in elderly is initiated by multiplefactors. These include impairment of the immune cell responses to inflammatorystimuli, age-related modification to the microenvironment, metabolic andhormonal systemic changes 1. Not to mention that chronicinflammatory state will contribute to developing several chronic diseases,obesity for example.
Such advanced age potentially contributes more to centralobesity which in turn cause insulin resistance 3.