Evidence map›Paper›PMID 35069556›Full record

Trial reportFrontiers in immunology2021

N-Formyl Methionine Peptide-Mediated Neutrophil Activation in Systemic Sclerosis.

Runa Kuley, Ryan D Stultz, Bhargavi Duvvuri, Ting Wang, Marvin J Fritzler, Roger Hesselstrand, J Lee Nelson, Christian Lood

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Effects of Melatonin andAntioxidants (Basel, Switzerland) · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. [Research progress on cellular metabolic reprogramming in skin fibrosis].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Review
  10. Review
  11. NETosis: A key player in autoimmunity, COVID-19, and long COVID.Journal of translational autoimmunity · 2025
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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

8 authors at 3 institutions in 3 countries.

Runa KuleyDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
Ryan D StultzDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
Bhargavi DuvvuriDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
Ting WangDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
Marvin J FritzlerDepartment of Biochemistry and Molecular Biology, University of Calgary, Calgary, AB, Canada.
Roger HesselstrandDepartment of Clinical Sciences Lund University, Section of Rheumatology, Lund, Sweden.
J Lee NelsonDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
Christian LoodDepartment of Medicine, Division of Rheumatology, University of Washington, Seattle, WA, United States.
University of Washington · USLund University · SEUniversity of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exaggerated neutrophil activation and formation of neutrophil extracellular traps (NETs) are reported in systemic sclerosis (SSc) but its involvement in SSc pathogenesis is not clear. In the present study we assessed markers of neutrophil activation and NET formation in SSc patients in relation to markers of inflammation and disease phenotype. Factors promoting neutrophil activation in SSc remain largely unknown. Among the neutrophil activating factors, mitochondrial-derived N-formyl methionine (fMet) has been reported in several autoinflammatory conditions. The aim of the current study is to assess whether SSc patients have elevated levels of fMet and the role of fMet in neutrophil-mediated inflammation on SSc pathogenesis. Markers of neutrophil activation (calprotectin, NETs) and levels of fMet were analyzed in plasma from two SSc cohorts (n=80 and n=20, respectively) using ELISA. Neutrophil activation assays were performed in presence or absence of formyl peptide receptor 1 (FPR1) inhibitor cyclosporin H. Elevated levels of calprotectin and NETs were observed in SSc patients as compared to healthy controls (p<0.0001) associating with SSc clinical disease characteristics. Further, SSc patients had elevated levels of circulating fMet as compared to healthy controls (p<0.0001). Consistent with a role for fMet-mediated neutrophil activation, fMet levels correlated with levels of calprotectin and NETs (r=0.34, p=0.002; r=0.29, p<0.01 respectively). Additionally, plasma samples from SSc patients with high levels of fMet induced

Indexed as

AdultAgedAged, 80 and overBiomarkersExtracellular TrapsFemaleHumansMaleMiddle AgedNeutrophil ActivationNeutrophilsN-Formylmethionine Leucyl-PhenylalanineScleroderma, SystemicBiomarkersN-Formylmethionine Leucyl-Phenylalanineautoimmunityclinical biomarkersmitochondrial peptidesneutrophil extracellular traps (NET)neutrophils (PMNs)systemic sclerosis

Identifiers

PMID35069556
PMCPMC8766990
OpenAlexW4205154650

What Socratic holds

Textmetadata
LicenceCC BY
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.