Immunity in the Progeroid Model of Cockayne Syndrome: Biomarkers of Pathological Aging

Author:

Zayoud Khouloud12,Chikhaoui Asma1,Kraoua Ichraf3,Tebourbi Anis4,Najjar Dorra1,Ayari Saker4,Safra Ines5,Kraiem Imen5,Turki Ilhem3,Menif Samia5,Yacoub-Youssef Houda1ORCID

Affiliation:

1. Laboratory of Biomedical Genomics and Oncogenetics (LR16IPT05), Institut Pasteur de Tunis, Université Tunis El Manar, El Manar I, Tunis 1002, Tunisia

2. Faculty of Sciences of Bizerte, Bizerte 7021, Tunisia

3. Department of Neuropediatrics, National Institute of Neurology Mongi Ben Hamida, Tunis 1007, Tunisia

4. Orthopedic and Trauma Surgery Department, Mongi Slim Hospital, La Marsa 2070, Tunisia

5. Laboratory of Molecular and Cellular Hematology (LR16IPT07), Institut Pasteur de Tunis, Université Tunis El Manar, El Manar I, Tunis 1002, Tunisia

Abstract

Cockayne syndrome (CS) is a rare autosomal recessive disorder that affects the DNA repair process. It is a progeroid syndrome predisposing patients to accelerated aging and to increased susceptibility to respiratory infections. Here, we studied the immune status of CS patients to determine potential biomarkers associated with pathological aging. CS patients, as well as elderly and young, healthy donors, were enrolled in this study. Complete blood counts for patients and donors were assessed, immune cell subsets were analyzed using flow cytometry, and candidate cytokines were analyzed via multi-analyte ELISArray kits. In CS patients, we noticed a high percentage of lymphocytes, an increased rate of intermediate and non-classical monocytes, and a high level of pro-inflammatory cytokine IL-8. In addition, we identified an increased rate of particular subtypes of T Lymphocyte CD8+ CD28− CD27−, which are senescent T cells. Thus, an inflammatory state was found in CS patients that is similar to that observed in the elderly donors and is associated with an immunosenescence status in both groups. This could explain the CS patients’ increased susceptibility to infections, which is partly due to an aging-associated inflammation process.

Funder

Ministry of Higher Education and Scientific Research

Projet Collaboratif Interne

MOBIDOC-753

PTR111-17

Publisher

MDPI AG

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