Metabolic pathways in immune senescence and inflammaging: Novel therapeutic strategy for chronic inflammatory lung diseases. An EAACI position paper from the Task Force for Immunopharmacology.
Franziska Roth-WalterIssssswan M AdcockCristina Benito-VillalvillaRodolfo BianchiniBjermer LeifGaetano CaramoriLuigi CariKian Fan ChungZuzana DiamantIbon Eguiluz GraciaEdward F KnolJesenak MilosFrancesca Levi-SchafferGiuseppe NocentiniCorina M BersetÓscar PalomaresFrank A RedegeldMilena SokolowskaBetty C A M van EschCristiana StellatoPublished in: Allergy (2023)
The accumulation of senescent cells drives inflammaging and increases morbidity of chronic inflammatory lung diseases. Immune responses are built upon dynamic changes in cell metabolism that supply energy and substrates for cell proliferation, differentiation, and activation. Metabolic changes imposed by environmental stress and inflammation on immune cells and tissue microenvironment are thus chiefly involved in the pathophysiology of allergic and other immune-driven diseases. Altered cell metabolism is also a hallmark of cell senescence, a condition characterized by loss of proliferative activity in cells that remain metabolically active. Accelerated senescence can be triggered by acute or chronic stress and inflammatory responses. In contrast, replicative senescence occurs as part of the physiological aging process and has protective roles in cancer surveillance and wound healing. Importantly, cell senescence can also change or hamper response to diverse therapeutic treatments. Understanding the metabolic pathways of senescence in immune and structural cells is therefore critical to detect, prevent, or revert detrimental aspects of senescence-related immunopathology, by developing specific diagnostics and targeted therapies. In this paper, we review the main changes and metabolic alterations occurring in senescent immune cells (macrophages, B cells, T cells). Subsequently, we present the metabolic footprints described in translational studies in patients with chronic asthma and chronic obstructive pulmonary disease (COPD), and review the ongoing preclinical studies and clinical trials of therapeutic approaches aiming at targeting metabolic pathways to antagonize pathological senescence. Because this is a recently emerging field in allergy and clinical immunology, a better understanding of the metabolic profile of the complex landscape of cell senescence is needed. The progress achieved so far is already providing opportunities for new therapies, as well as for strategies aimed at disease prevention and supporting healthy aging.
Keyphrases
- dna damage
- chronic obstructive pulmonary disease
- endothelial cells
- single cell
- stress induced
- cell therapy
- induced apoptosis
- clinical trial
- oxidative stress
- immune response
- stem cells
- cell proliferation
- cell cycle arrest
- public health
- randomized controlled trial
- magnetic resonance
- wound healing
- drug delivery
- signaling pathway
- inflammatory response
- climate change
- cystic fibrosis
- cell death
- dendritic cells
- risk assessment
- toll like receptor
- endoplasmic reticulum stress
- mesenchymal stem cells