Innate immune perturbations, accumulating DAMPs and inflammasome dysregulation: a ticking time bomb in ageing

Kapetanovic, Ronan, Bokil, Nilesh J. and Sweet, Matthew J. (2015) Innate immune perturbations, accumulating DAMPs and inflammasome dysregulation: a ticking time bomb in ageing. Ageing Research Reviews, 24 40-53. doi:10.1016/j.arr.2015.02.005


Author Kapetanovic, Ronan
Bokil, Nilesh J.
Sweet, Matthew J.
Title Innate immune perturbations, accumulating DAMPs and inflammasome dysregulation: a ticking time bomb in ageing
Journal name Ageing Research Reviews   Check publisher's open access policy
ISSN 1872-9649
1568-1637
Publication date 2015
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.arr.2015.02.005
Volume 24
Start page 40
End page 53
Total pages 14
Place of publication Shannon, Clare Ireland
Publisher Elsevier Ireland
Collection year 2016
Language eng
Abstract Ageing has pronounced effects on the immune system, including on innate immune cells. Whilst most studies suggest that total numbers of different innate immune cell populations do not change dramatically during ageing, many of their functions such as phagocytosis, antigen presentation and inflammatory molecule secretion decline. In contrast, many endogenous damage-associated molecular patterns (DAMPs) accumulate during ageing. These include reactive oxygen species (ROS) released from damaged mitochondria, extracellular nucleotides like ATP, high mobility group box (HMGB) 1 protein, oxidized low density lipoprotein, amyloid-beta (Aβ), islet amyloid polypeptide and particulates like monosodium urate (MSU) crystals and cholesterol crystals. Some of these DAMPs trigger the activation of inflammasomes, cytosolic danger sensing signalling platforms that drive both the maturation of specific pro-inflammatory mediators such as IL-1β, as well as the initiation of pro-inflammatory pyroptotic cell death. Herein, we review the evidence that dysregulated inflammasome activation, via altered innate immune cell functions and elevated levels of DAMPs, contributes to the establishment of chronic, low-grade inflammation (characterized by elevated levels of IL-6 and C-reactive protein) and the development of age-related pathological processes.
Keyword Autophagy
DAMPs
Inflammasome
Inflammation
Nod-like receptors
Pattern recognition receptors
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2016 Collection
Institute for Molecular Bioscience - Publications
 
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