Evidence map›Paper›PMID 18194266›Full record

ArticleImmunology2008

Microbicidal protein psoriasin is a multifunctional modulator of neutrophil activation.

Yan Zheng, François Niyonsaba, Hiroko Ushio, Shigaku Ikeda, Isao Nagaoka, Ko Okumura, Hideoki Ogawa

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 92 citations in OpenAlex.

  1. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Pathogenic role of S100 proteins in psoriasis.Frontiers in immunology · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. The Immunogenetics of Morphea and Lichen Sclerosus.Advances in experimental medicine and biology · 2022
    Review
  11. Keratinocytes: innate immune cells in atopic dermatitis.Clinical and experimental immunology · 2021
    Review
  12. Review
  13. Article
  14. Alarmins and immunity.Immunological reviews · 2017
    Review
  15. Article
  16. Review
  17. Article
  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

7 authors at 1 institution in 1 country.

Yan ZhengDepartment of Dermatology, Atopy Allergy Research Centre, Juntendo University School of Medicine, Tokyo, Japan.
François Niyonsaba
Hiroko Ushio
Shigaku Ikeda
Isao Nagaoka
Ko Okumura
Hideoki Ogawa
Juntendo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As effector cells in host defence, neutrophils actively destroy invading microorganisms via a potent antimicrobial arsenal composed of oxidants and antimicrobial peptides. Psoriasin, an Escherichia coli-cidal antimicrobial protein, has been found to be overexpressed in psoriasis, a skin disease characterized by infiltration of neutrophils. In addition to its microbicidal activities and chemotaxis of neutrophils reported previously, we hypothesized that psoriasin might regulate other neutrophil functions such as cytokine and chemokine production, reactive oxygen species generation, and release of antimicrobial peptides. In the current study, we demonstrate that psoriasin activates neutrophils to produce a range of cytokines and chemokines including interleukin-6 (IL-6), IL-8/CXCL8, tumour necrosis factor-alpha, macrophage inflammatory protein-1alpha (MIP-1alpha)/CCL3, MIP-1beta/CCL4 and MIP-3alpha/CCL20. Furthermore, psoriasin induces phosphorylation of mitogen-activated protein kinase p38 and extracellular signal-regulated kinase (ERK), but not c-Jun N-terminal kinase (JNK), both of which are required for the production of cytokines and chemokines as evidenced by the inhibitory effects of p38 and ERK inhibitors on psoriasin-mediated neutrophil activation. Moreover, psoriasin stimulates the generation of reactive oxygen species from neutrophils, most likely via nicotinamide adenine dinucleotide phosphate oxidase activation. Finally, we demonstrate that psoriasin enhances messenger RNA expression of alpha-defensins, termed human neutrophil peptides (HNP) 1 to 3, and induces their extracellular release. Besides its antimicrobial properties, therefore, psoriasin may contribute to innate immunity through enhancing neutrophil host defence functions at sites of inflammation or infection.

Indexed as

alpha-DefensinsApoptosisCalciumCalcium-Binding ProteinsCell DegranulationCells, CulturedChemokinesCytokinesExtracellular Signal-Regulated MAP KinasesGene Expression RegulationHumansNADPH OxidasesNeutrophil ActivationNeutrophilsp38 Mitogen-Activated Protein KinasesPhosphorylationalpha-DefensinsCalciumCalcium-Binding ProteinsChemokinesCytokinesExtracellular Signal-Regulated MAP KinasesNADPH Oxidasesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesS100A7 protein, humanS100 Calcium Binding Protein A7S100 ProteinsZinc

Identifiers

PMID18194266
PMCPMC2440830
OpenAlexW2130850468

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.