Evidence map›Paper›PMID 30537894›Full record

ArticleInnate immunity2019

Olfactomedin 4 marks a subset of neutrophils in mice.

Matthew N Alder, Jaya Mallela, Amy M Opoka, Patrick Lahni, David A Hildeman, Hector R Wong

Open access · hybridAbstract read
In one paragraph

Article in Innate immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.4field-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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. A neutrophil subset defined by intracellular olfactomedin 4 is associated with mortality in sepsis.American journal of physiology. Lung cellular and molecular physiology · 2021
    Trial
  2. Article
  3. Article
  4. Olfactomedin-4Infection and immunity · 2026
    Article
  5. The Ly6gCancer communications (London, England) · 2026
    Article
  6. Article
  7. Olfactomedin-4 elevation in pediatric acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Targeting Neutrophil βBiomolecules · 2023
    Review
  16. CD115Communications biology · 2023
    Article
  17. Review
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Matthew N Alder1 Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, USA.ORCID 0000-0003-2879-6576
Jaya Mallela1 Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, USA.
Amy M Opoka1 Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, USA.
Patrick Lahni1 Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, USA.
David A Hildeman2 Division of Immunobiology, Cincinnati Children's Hospital Medical Center, USA.
Hector R Wong1 Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center, USA.
Cincinnati Children's Hospital Medical Center · US

Funding

Supplement for MIRA award_Wong_2021R35GM126943 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI ALDER, MATTHEW N · 2018 to 2022
$2.7M
The Role of Olfactomedin 4 in Septic ShockK08GM124298 · NIGMS · CINCINNATI CHILDRENS HOSP MED CTR · PI ALDER, MATTHEW N · 2017 to 2020
$758k
NIGMS NIH HHS K08 GM124298NIGMS NIH HHS R35 GM126943
6 · The paper itself

Abstract

Neutrophils are the most abundant immune cell of the innate immune system and participate in essential immune functions. Heterogeneity within neutrophils has been documented, but it is difficult to distinguish if these are altered activation states of a single population or separate subpopulations of neutrophils determined at the time of differentiation. Several groups have identified a subset of human neutrophils that express olfactomedin 4 (OLFM4) and increased OLFM4+ neutrophils during sepsis is correlated with worse outcome, suggesting these neutrophils or the OLFM4 they secrete may be pathogenic. We tested if mice could be used as a model to study OLFM4+ neutrophils. We found the OLFM4 expressing subset of neutrophils is conserved in mice. Depending on the strain, 7-35% of murine neutrophils express OLFM4 and expression is determined early in neutrophil differentiation. OLFM4+ neutrophils phagocytose and transmigrate with similar efficiency as OLFM4- neutrophils. Here we show that within neutrophil extracellular traps (NETs) OLFM4+ and OLFM4- neutrophils undergo NETosis and OLFM4 colocalizes. Finally, we generated an OLFM4 null mouse and show that these mice are protected from death when challenged with sepsis, providing further evidence that the OLFM4 expressing subpopulation of neutrophils, or the OLFM4 they secrete, may be pathogenic during overwhelming infection.

Indexed as

AnimalsApoptosisCell DifferentiationCells, CulturedExtracellular TrapsGlycoproteinsHumansImmunity, InnateMiceMice, Inbred BALB CMice, Inbred C57BLMutationNeutrophilsPhagocytosisSepsisGlycoproteinsolfactomedin 4, mouseheterogeneityinflammationNeutrophilsolfactomedinsepsis

Identifiers

PMID30537894
PMCPMC6661892
OpenAlexW2905179255

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.