Immunosenescence in neurocritical care

Abstract

Background: Several advanced and developing countries are now entering a superaged society, in which the percentage of elderly people exceeds 20% of the total population. In such an aging society, the number of age-related diseases such as malignant tumors, diabetes, and severe infections including sepsis is increasing, and patients with such disorders often find themselves in the ICU.

Main body: Age-related diseases are closely related to age-induced immune dysfunction, by which reductions in the efficiency and specificity of the immune system are collectively termed "immunosenescence." The most noticeable is a decline in the antigen-specific acquired immune response. The exhaustion of T cells in elderly sepsis is related to an increase in nosocomial infections after septicemia, and even death over subacute periods. Another characteristic is that senescent cells that accumulate in body tissues over time cause chronic inflammation through the secretion of proinflammatory cytokines, termed senescence-associated secretory phenotype. Chronic inflammation associated with aging has been called "inflammaging," and similar age-related diseases are becoming an urgent social problem.

Conclusion: In neuro ICUs, several neuro-related diseases including stroke and sepsis-associated encephalopathy are related to immunosenescence and neuroinflammation in the elderly. Several advanced countries with superaged societies face the new challenge of improving the long-term prognosis of neurocritical patients.

Keywords: Elderly; Immune paralysis; Immunosenescence; Sepsis.

Fig. 1

Changes in bone marrow/thymus accompanying aging and changes in immune response cells. Although the number of stem cells in the bone marrow is not affected by aging, differentiation into common lymphoid progenitor cells decreases and shifts to differentiation into myeloid-type common progenitor cells. Therefore, differentiation into lymphoid cells (T cells, B cells) decreases, and differentiation into myeloid cells (granulocytes/monocytes) increases. The thymus, which is the site of the differentiation and maturation of T cells, atrophies with age. Therefore, in young people, naive T cells predominate; however, with age, there is a shift to dominant T cells (memory T cells), which is activated by antigen stimulation or some internal factor. HSCs, hematopoietic stem cells; CMP, common myeloid progenitor; CLP, common lymphoid progenitor

Fig. 2

Age-related changes in innate immune effector cells

Fig. 3

Age-related changes in adaptive immune effector cells

Fig. 4

Aging of somatic cells and immune effector cells. SAPS, senescence-associated secretory phenotype

Fig. 5

Mechanism of sepsis-associated encephalopathy