Evidence map›Paper›PMID 35314351›Full record

ArticleBiochimica et biophysica acta. Molecular basis of disease2022

Oxidative stress and endogenous DNA damage in blood mononuclear cells may predict anti-SARS-CoV-2 antibody titers after vaccination in older adults.

Panagiotis A Ntouros, Evrydiki Kravvariti, Nikolaos I Vlachogiannis, Maria Pappa, Ioannis P Trougakos, Evangelos Terpos, Maria G Tektonidou, Vassilis L Souliotis, Petros P Sfikakis

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In one paragraph

Article in Biochimica et biophysica acta. Molecular basis of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Panagiotis A NtourosFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece. Electronic address: panantou@med.uoa.gr.
Evrydiki KravvaritiFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Postgraduate Medical Studies in the Physiology of Aging and Geriatric Syndromes, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Nikolaos I VlachogiannisFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Maria PappaFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Athens, Greece.
Evangelos TerposDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Maria G TektonidouFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Vassilis L SouliotisFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Institute of Chemical Biology, National Hellenic Research Foundation, Athens, Greece.
Petros P SfikakisFirst Department of Propaedeutic Internal Medicine and Joint Rheumatology Program, National and Kapodistrian University of Athens Medical School, Athens, Greece; Postgraduate Medical Studies in the Physiology of Aging and Geriatric Syndromes, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece. Electronic address: psfikakis@med.uoa.gr.
National and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune senescence in the elderly has been associated with chronic oxidative stress and DNA damage accumulation. Herein we tested the hypothesis that increased endogenous DNA damage and oxidative stress in peripheral blood mononuclear cells of older adults associate with diminished humoral immune response to SARS-CoV-2 vaccination. Increased oxidative stress and DNA double-strand breaks (DSBs) were detected in 9 non-immunocompromised individuals aged 80-96 years compared to 11 adults aged 27-44 years, before, as well as on days 1 and 14 after the first dose, and on day 14 after the second dose of the BNT162B2-mRNA vaccine (all p < 0.05). SARS-CoV-2 vaccination induced a resolvable increase in oxidative stress and DNA damage, but individual DSB-repair efficiency was unaffected by vaccination irrespective of age, confirming vaccination safety. Individual titers of anti-Spike-Receptor Binding Domain (S-RBD)-IgG antibodies, and the neutralizing capacity of circulating anti-SARS-CoV-2 antibodies, measured on day 14 after the second dose in all participants, correlated inversely with the corresponding pre-vaccination endogenous oxidative stress and DSB levels (all p < 0.05). In particular, a strong inverse correlation of individual pre-vaccination DSB levels with both the respective anti-S-RBD-IgG antibodies titers (r = -0.867) and neutralizing capacity of circulating anti-SARS-CoV-2 antibodies (r = -0.983) among the 9 older adults was evident. These findings suggest that humoral responses to SARS-CoV-2 vaccination may be weaker when immune cells are under oxidative and/or genomic stress. Whether such measurements may serve as biomarkers of vaccine efficacy in older adults warrants further studies.

Indexed as

BNT162 VaccineCOVID-19AdultAgedAged, 80 and overCOVID-19 VaccinesDNA DamageHumansLeukocytes, MononuclearmRNA VaccinesOxidative StressSARS-CoV-2VaccinationVaccines, SyntheticBNT162 VaccineCOVID-19 VaccinesmRNA VaccinesVaccines, SyntheticDNA damage responseHumoral responsemRNA vaccinationOxidative stressSARS-CoV-2 antibody

Identifiers

PMID35314351
PMCPMC8930778
OpenAlexW4220742958

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.