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Title (en)
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
Language
English
Description (en)
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.
Keywords (en)
Humans; Cellular Senescence Drug Effects; Metabolic Networks and Pathways; Animals; Chronic Disease; Inflammation Metabolism Immunology; Lung Diseases Etiology Drug Therapy Metabolism Immunology; Pulmonary Disease, Chronic Obstructive Metabolism Drug Therapy Immunology; Aging Immunology Metabolism
DOI
10.1111/all.15977
Author of the digital object
Franziska Roth-Walter  (University of Veterinary Medicine, Vienna / Medical University of Vienna)
C. Stellato  (University of Salerno)
B. C. A. M. Van Esch  (Utrecht University)
M. Sokolowska  (University of Zurich / CK-CARE)
F. Redegeld  (Utrecht University)
O. Palomares  (Universidad Complutense de Madrid)
L. O'Mahony  (University College Cork)
G. Nocentini  (University of Perugia)
F. Levi-Schaffer  (Hebrew University of Jerusalem)
M. Jesenak  (Comenius University Bratislava)
E. F. Kohl  (University Medical Center Utrecht)
I. Eguiluz-Gracia  (Instituto de Investigación Biomédica de Málaga)
Z. Diamant  (Skåne University Hospital / Charles University / University of Groningen)
I. M. Adcock  (Imperial College London)
C. Benito-Villalvilla  (Universidad Complutense de Madrid)
Rodolfo Bianchini  (University of Veterinary Medicine Vienna)
L. Bjermer  (Lund University)
G. Caramori  (University of Parma)
L. Cari  (University of Perugia)
K. F. Chung  (Imperial College London)
Format
application/pdf
Size
2.0 MB
Licence Selected
CC BY-NC 4.0 International
Type of publication
Article
Name of Publication (de)
Allergy
Pages or Volume
34
Volume
79
Number
5
From Page
1089
To Page
1122
Publisher
Wiley
Publication Date
2023