Evidence map›Paper›PMID 42065235›Full record

ArticleThe Journal of clinical investigation2026

Secreted phospholipase PLA2G5 acts as a hemolytic factor in sepsis.

Michihiro Takahama, Krysta S Wolfe, Gabriella Richey, Madison Plaster, Anna Czapar, Fabian Hernandez, Denis Cipurko, Tatsuki Ueda, Yoshimi Miki, Yuki Nagasaki and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 2026. 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. Article
  2. Review
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

16 authors.

Michihiro TakahamaPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Krysta S WolfePulmonary and Critical Care, and.
Gabriella RicheyPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Madison PlasterPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Anna CzaparSection of Infectious Diseases and Global Health, Department of Medicine, The University of Chicago Medical Center, Chicago, Illinois, USA.
Fabian HernandezPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Denis CipurkoPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Tatsuki UedaPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.
Yoshimi MikiLipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Yuki NagasakiLipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Yoshitaka TaketomiLipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tatsuya SaitohLaboratory of Bioresponse Regulation, Graduate School of Pharmaceutical Sciences, The University of Osaka, Osaka, Japan.
Tadafumi KawamotoSchool of Dental Medicine, Tsurumi University, Yokohama, Japan.
Steven M DudekDivision of Pulmonary, Critical Care, Sleep and Allergy, Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, USA.
Makoto MurakamiLipid Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Nicolas ChevrierPritzker School of Molecular Engineering, The University of Chicago, Chicago, Illinois, USA.

Funding

Molecular Mechanisms of Adjuvant Triplet CombinationsU01AI160418 · NIAID · UNIVERSITY OF CHICAGO · PI CHEVRIER, NICOLAS · 2021 to 2025
$3.1M
Building a Predictive Framework for Adjuvant Combinatorics in Vaccine DevelopmentDP2AI145100 · NIAID · UNIVERSITY OF CHICAGO · PI CHEVRIER, NICOLAS · 2018 to 2018
$2.4M
Spatiomolecular Profiling of Human Cancer at ScaleR33CA297902 · NCI · UNIVERSITY OF CHICAGO · PI Nicolas Chevrier · 2025 to 2026
$743k
NCI NIH HHS R33 CA297902NIAID NIH HHS DP2 AI145100NIAID NIH HHS U01 AI160418
6 · The paper itself

Abstract

Sepsis is a systemic response to infection with life-threatening consequences such as hemolysis, a predictor of mortality risks for the disease. Here, by measuring organism-wide changes in gene expression, we discovered that the secreted phospholipase PLA2G5 is induced in colon cell types during sepsis. The genetic deletion of Pla2g5 and treatment with a PLA2G5 antibody were both associated with protection from lethal sepsis. Treatment with a PLA2G5 antibody during sepsis was associated with increased splenic red pulp macrophages and improved iron homeostasis, linking PLA2G5 to red blood cell homeostasis during sepsis. Mechanistically, bloodborne PLA2G5 led to intravascular hemolysis through its lipolytic activity on red blood cell membranes. In humans with sepsis due to bacterial, fungal, or viral infections, the serum level of PLA2G5 was elevated and predictive of disease severity and mortality. We conclude that sepsis corrupts PLA2G5 into becoming an intravascular hemolytic factor which is toxic for host red blood cells.

Indexed as

ErythrocytesGroup V Phospholipases A2HemolysisSepsisAnimalsFemaleHumansMaleMiceMice, KnockoutGroup V Phospholipases A2Bacterial infectionsBiomarkersExpression profilingInfectious diseaseInflammation

Identifiers

PMID42065235
PMCPMC13132393

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Registered trials

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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.