Evidence map›Paper›PMID 40322970›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

Enhanced Production of Lipid Mediators in Plasma and Activation of DNA Damage Pathways in PBMCs Are Correlated With the Severity of Ancestral SARS-CoV-2 Infection.

Jeffrey A Tomalka, Anna Owings, Michelle Galeas-Pena, Carly G K Ziegler, Tanya O Robinson, Thomas G Wichman, Hannah Laird, Haley B Williams, Neha S Ghaliwal, Steven Everman and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Jeffrey A TomalkaDepartment of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
Anna OwingsDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Michelle Galeas-PenaDepartment of Medicine, Section of Gastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, Louisiana, USA.
Carly G K ZieglerProgram in Health Sciences & Technology, Harvard Medical School & MIT, Boston, Massachusetts, USA.
Tanya O RobinsonDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Thomas G WichmanDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Hannah LairdDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Haley B WilliamsDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Neha S GhaliwalDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Steven EvermanDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Yousaf ZafarDepartment of Medicine, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Jaclyn M L WalshBroad Institute of MIT and Harvard, Cambridge, Massachusetts, USA.
Alex K ShalekProgram in Health Sciences & Technology, Harvard Medical School & MIT, Boston, Massachusetts, USA.
Bruce H HorwitzDepartment of Immunology, Harvard Medical School, Boston, Massachusetts, USA.
Jose Ordovas-MontanesRagon Institute of MGH, MIT, and Harvard, Cambridge, Massachusetts, USA.
Sarah C GloverDepartment of Medicine, Section of Gastroenterology and Hepatology, Tulane University School of Medicine, New Orleans, Louisiana, USA.
Yann GibertDepartment of Cell and Molecular Biology, University of Mississippi Medical Center, Jackson, Mississippi, USA.

Funding

Tracking and Evaluation CoreU54GM115428 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$3.6M
Project 003 - Lorena AmaralP20GM121334 · UNIVERSITY OF MISSISSIPPI MED CTR · 2025 to 2025
$2.6M
Initiation of immune responses to SARS COV2 in the oral cavity and upper airwayR01DE031928 · TULANE UNIVERSITY OF LOUISIANA · 2025 to 2025
$742k
HHS | NIH | National Institute of Dental and Craniofacial Research (NIDR) R01DE31928HHS | NIH | National Institute of General Medical Sciences (NIGMS) P20GM104357HHS | NIH | National Institute of General Medical Sciences (NIGMS) P20GM121334HHS | NIH | National Institute of General Medical Sciences (NIGMS) U54GM115428NIDCR NIH HHS R01 DE031928NIGMS NIH HHS P20 GM104357NIGMS NIH HHS P20 GM121334NIGMS NIH HHS U54 GM115428
6 · The paper itself

Abstract

Many questions remain unanswered regarding the implication of genetics and lipid metabolites with severe SARS-CoV-2 infections. We performed bulk RNA-seq and a total fatty acid panel analysis on PBMCs and plasma collected from 10 infected and 10 uninfected patients. Univariate comparison of lipid metabolites using the Mann-Whitney U-test revealed that six lipid metabolites were significantly increased in COVID-19 patients, including the lipid mediators arachidonic acid (AA) and eicosapentaenoic acid (EPA), which both give rise to eicosanoids. Key lipids implicated in inflammation, including AA and EPA, along with the fatty acids DHA and DPA, were significantly and positively correlated to the WHO disease severity score. Analysis of our bulk RNA-seq dataset demonstrated distinct transcriptional profiles leading to a segregation of COVID-19 patients based on the WHO score. Ontology, KEGG, and Reactome analysis identified several key pathways and nodes that were enriched for genes related to innate immunity, interactions between lymphoid and nonlymphoid cells, interleukin signaling, and subsequent DNA damage pathways. EPA levels correlated with heightened cell cycling and DNA damage pathways observed in patients with a high WHO score. We studied gene expression in nasopharyngeal swabs from 58 healthy and COVID-19 participants and identified that genes implicated in eicosanoid synthesis, such as alox5, alox12, and alox15B, were specifically up-regulated in high WHO score patients in several cell types of the nasopharynx, especially goblet cells across different viral variants (Deta and Omicron). Using published nasal scRNA-seq datasets from COVID-19 patients, we evaluated the expression of genes implicated in eicosanoid synthesis, such as ALOX5, ALOX15, and ALOX15B, across nasal cell types and COVID-19 severity groups. Altogether, our study highlights the fact that the increase in specific lipids implicated in inflammation and the genes required for their synthesis correlated with the severity of the SARS-CoV-2 infection.

Indexed as

COVID-19DNA DamageLeukocytes, MononuclearLipid MetabolismLipidsSARS-CoV-2AdultAgedArachidonic AcidEicosanoidsEicosapentaenoic AcidFemaleHumansMaleMiddle AgedSeverity of Illness IndexArachidonic AcidEicosanoidsEicosapentaenoic AcidLipidsDNA damageeicosanoidsfatty acidlipidomicsRNAseqSARS‐CoV‐2

Identifiers

PMID40322970
PMCPMC12904103

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.