Evidence map›Paper›PMID 29180999›Full record

ArticleFrontiers in immunology2017

Alarmin S100A8 Activates Alveolar Epithelial Cells in the Context of Acute Lung Injury in a TLR4-Dependent Manner.

Deblina Chakraborty, Stefanie Zenker, Jan Rossaint, Anna Hölscher, Michele Pohlen, Alexander Zarbock, Johannes Roth, Thomas Vogl

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

41 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Cytosolic proliferating cell nuclear antigen (PCNA) orchestrates neutrophil hyperactivation in COVID-19.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Post-burn Lung Inflammation Is Associated With Induction of Pulmonary Cathelicidin-related Antimicrobial Peptide and S100a8 in Mice.Journal of burn care & research : official publication of the American Burn Association · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mutation-Driven S100A8 Overexpression Confers Aberrant Phenotypes in Type 1International journal of molecular sciences · 2023
    Article
  19. Observational
  20. IFN-American journal of respiratory cell and molecular biology · 2023
    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 1 institution in 1 country.

Deblina ChakrabortyInstitute of Immunology, University of Münster, Münster, Germany.
Stefanie ZenkerInstitute of Immunology, University of Münster, Münster, Germany.
Jan RossaintDepartment of Anaesthesiology and Intensive Care, University of Münster, Münster, Germany.
Anna HölscherInstitute of Immunology, University of Münster, Münster, Germany.
Michele PohlenInstitute of Immunology, University of Münster, Münster, Germany.
Alexander ZarbockDepartment of Anaesthesiology and Intensive Care, University of Münster, Münster, Germany.
Johannes RothInstitute of Immunology, University of Münster, Münster, Germany.
Thomas VoglInstitute of Immunology, University of Münster, Münster, Germany.
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alveolar epithelial cells (AECs) are an essential part of the respiratory barrier in lungs for gas exchange and protection against pathogens. Damage to AECs occurs during lung injury and PAMPs/DAMPs have been shown to activate AECs. However, their interplay as well as the mechanism of AECs' activation especially by the alarmin S100A8/A9 is unknown. Thus, our aim was to study the mechanism of activation of AECs (type I and type II) by S100A8 and/or lipopolysaccharide (LPS) and to understand the role of endogenous S100A8/A9 in neutrophil recruitment in the lung. For our studies, we modified a previous protocol for isolation and culturing of murine AECs. Next, we stimulated the cells with S100A8 and/or LPS and analyzed cytokine/chemokine release. We also analyzed the contribution of the known S100-receptors TLR4 and RAGE in AEC activation. In a murine model of lung injury, we investigated the role of S100A8/A9 in neutrophil recruitment to lungs. S100A8 activates type I and type II cells in a dose- and time-dependent manner which could be quantified by the release of IL-6, KC, and MCP-1. We here clearly demonstrate that AEC s are activated by S100A8

Indexed as

damage-associated molecular patternsIL-6neutrophilsS100A8TLR4type I alveolar epithelial cellstype II alveolar epithelial cells

Identifiers

PMID29180999
PMCPMC5693860
OpenAlexW2768088874

What OpenQuestion 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 OpenQuestion graph.