Format

Send to

Choose Destination
Clin Immunol. 2019 Mar;200:43-54. doi: 10.1016/j.clim.2019.02.002. Epub 2019 Feb 5.

Immune aging in diabetes and its implications in wound healing.

Author information

1
Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal; INEB - Instituto Nacional de Engenharia Biomédica, University of Porto, Porto, Portugal; i3S - Instituto de Investigação e Inovação em Saúde, University of Porto, Porto, Portugal. Electronic address: joao.moura@i3s.up.pt.
2
i3S - Instituto de Investigação e Inovação em Saúde, University of Porto, Porto, Portugal; IBMC - Instituto de Biologia Celular e Molecular, University of Porto, Porto, Portugal; Immunethep, Biocant Park, Cantanhede, Portugal.
3
Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
4
Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal; Instituto de Investigação Interdisciplinar, University of Coimbra, Coimbra, Portugal; Department of Geriatrics, University of Arkansas for Medical Sciences and Arkansas Children's Research Institute, Little Rock, AR, United States.

Abstract

Immune systems have evolved to recognize and eliminate pathogens and damaged cells. In humans, it is estimated to recognize 109 epitopes and natural selection ensures that clonally expanded cells replace unstimulated cells and overall immune cell numbers remain stationary. But, with age, it faces continuous repertoire restriction and concomitant accumulation of primed cells. Changes shaping the aging immune system have bitter consequences because, as inflammatory responses gain intensity and duration, tissue-damaging immunity and inflammatory disease arise. During inflammation, the glycolytic flux cannot cope with increasing ATP demands, limiting the immune response's extent. In diabetes, higher glucose availability stretches the glycolytic limit, dysregulating proteostasis and increasing T-cell expansion. Long-term hyperglycemia exerts an accumulating effect, leading to higher inflammatory cytokine levels and increased cytotoxic mediator secretion upon infection, a phenomenon known as diabetic chronic inflammation. Here we review the etiology of diabetic chronic inflammation and its consequences on wound healing.

KEYWORDS:

Chronic inflammation; diabetes; immune aging; wound healing

PMID:
30735729
DOI:
10.1016/j.clim.2019.02.002

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center