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With advancing age, the human body encounters various
dynamic adjustments. Immunosenescene, a term used to describe age-related
impairments in the immune system, is featured as an imbalance between inflammatory
and non-inflammatory mediators. This imbalance will dysregulate adaptive immunity
and activate low-grade inflammatory state and make the body more vulnerable to
autoimmune diseases 1. These changes are caused by the loss of
ability of hematopoietic stem cells (HSCs) to produce lymphoid progenitors and in
contrary shifting toward myeloid progenitors. Not only this, but also dysfunction
in monocytes, macrophages, neutrophils and dendritic cells is noted. As a
result, levels of naïve T and B cells as well as T-cell receptor (TCR) and
B-cell receptor (BCR) will be significantly decreased. To emphasize more on
macrophages, blood monocyte from aged subjects showed substantial decrease in
levels of TNF-a and IL-6 production, impaired phagocytosis, reduced chemotaxis,
and reduce MHC class 2 expression 1. Aging in particular can mimic
macrophage polarization in the presence of inflammatory factors which shift the
polarization from M2 to M1. Nevertheless, macrophages in adipose tissue of lean
subjects mainly express M2 phenotype, in contrast, obese subjects showed higher
levels on M1 phenotype and higher levels of CD4+ and CD8+ T cells as well 1.


Another study compared macrophage polarization of splenocytes in young
and aged mice after LPS stimulation, IFNg, TNF-a, and IL-4. After stimulation, noticeable
reduction 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 mice
compared to young mice 2.

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Certainly, chronic inflammation in elderly is initiated by multiple
factors. These include impairment of the immune cell responses to inflammatory
stimuli, age-related modification to the microenvironment, metabolic and
hormonal systemic changes 1. Not to mention that chronic
inflammatory state will contribute to developing several chronic diseases,
obesity for example. Such advanced age potentially contributes more to central
obesity which in turn cause insulin resistance 3.


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