Evidence map›Paper›PMID 27064756›Full record

ArticleAmerican journal of respiratory cell and molecular biology2016

Epithelial Cell-Derived Secreted and Transmembrane 1a Signals to Activated Neutrophils during Pneumococcal Pneumonia.

Hirofumi Kamata, Kazuko Yamamoto, Gregory A Wasserman, Mary C Zabinski, Constance K Yuen, Wing Yi Lung, Adam C Gower, Anna C Belkina, Maria I Ramirez, Jane C Deng and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Optimizing Neutrophil Recruitment to Tackle Bacterial Infections.American journal of respiratory cell and molecular biology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023
    Review
  12. Article
  13. Article
  14. Neutrophil Recruitment in Pneumococcal Pneumonia.Frontiers in cellular and infection microbiology · 2022
    Review
  15. Sectm1a Facilitates Protection against Inflammation-Induced Organ Damage through Promoting TRM Self-Renewal.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Unique Roles forFrontiers in immunology · 2020
    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

13 authors at 6 institutions in 4 countries.

Hirofumi Kamata1 Pulmonary Center.
Kazuko Yamamoto1 Pulmonary Center.
Gregory A Wasserman1 Pulmonary Center.
Mary C Zabinski1 Pulmonary Center.
Constance K Yuen4 Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California.
Wing Yi Lung4 Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California.
Adam C Gower5 Clinical and Translational Science Institute, and.
Anna C BelkinaDepartments of 3 Microbiology.
Maria I Ramirez1 Pulmonary Center.
Jane C Deng4 Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, California.
Lee J Quinton1 Pulmonary Center.
Matthew R Jones1 Pulmonary Center.
Joseph P Mizgerd1 Pulmonary Center.
Pulmonary Associates · USUniversity of California, Los Angeles · USEmory University Hospital · USBoston University · USMicrobiology Society · GBSouthern California Clinical and Translational Science Institute · US

Funding

NF-KB and Innate Immunity in the LungsR01HL068153 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI MIZGERD, JOSEPH P · 2003 to 2016
$5.1M
Lung-resident antibacterial heterotypic immunityR01AI115053 · NIAID · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MIZGERD, JOSEPH P · 2015 to 2023
$4.0M
Regulation and function of STAT3 during pneumoniaR01HL079392 · NHLBI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI MIZGERD, JOSEPH P · 2005 to 2015
$4.0M
Boston University Clinical and Translational Science Institute - U ProgramU54TR001012 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CENTER, DAVID M. · 2014 to 2014
$3.9M
The Biology of LIF During PneumoniaR01HL111449 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QUINTON, LEE · 2012 to 2020
$3.7M
MicroRNA uridylation by Zcchc11 regulates pulmonary inflammationR01HL104053 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI JONES, MATTHEW ROBERT · 2010 to 2014
$2.0M
Lung-Liver Axis During PneumoniaR00HL092956 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI QUINTON, LEE · 2010 to 2012
$745k
NCATS NIH HHS U54 TR001012NHLBI NIH HHS R00 HL092956NHLBI NIH HHS R01 HL068153NHLBI NIH HHS R01 HL079392NHLBI NIH HHS R01 HL104053NHLBI NIH HHS R01 HL111449NIAID NIH HHS R01 AI115053
6 · The paper itself

Abstract

Airway epithelial cell responses are critical to the outcome of lung infection. In this study, we aimed to identify unique contributions of epithelial cells during lung infection. To differentiate genes induced selectively in epithelial cells during pneumonia, we compared genome-wide expression profiles from three sorted cell populations: epithelial cells from uninfected mouse lungs, epithelial cells from mouse lungs with pneumococcal pneumonia, and nonepithelial cells from those same infected lungs. Of 1,166 transcripts that were more abundant in epithelial cells from infected lungs compared with nonepithelial cells from the same lungs or from epithelial cells of uninfected lungs, 32 genes were identified as highly expressed secreted products. Especially strong signals included two related secreted and transmembrane (Sectm) 1 genes, Sectm1a and Sectm1b. Refinement of sorting strategies suggested that both Sectm1 products were induced predominantly in conducting airway epithelial cells. Sectm1 was induced during the early stages of pneumococcal pneumonia, and mutation of NF-κB RelA in epithelial cells did not diminish its expression. Instead, type I IFN signaling was necessary and sufficient for Sectm1 induction in lung epithelial cells, mediated by signal transducer and activator of transcription 1. For target cells, Sectm1a bound to myeloid cells preferentially, in particular Ly6G(bright)CD11b(bright) neutrophils in the infected lung. In contrast, Sectm1a did not bind to neutrophils from uninfected lungs. Sectm1a increased expression of the neutrophil-attracting chemokine CXCL2 by neutrophils from the infected lung. We propose that Sectm1a is an epithelial product that sustains a positive feedback loop amplifying neutrophilic inflammation during pneumococcal pneumonia.

Indexed as

Neutrophil ActivationSignal TransductionAnimalsChemokine CXCL2Electric ConductivityEpithelial CellsGene Expression RegulationInterferon Type ILungMembrane ProteinsMice, Inbred C57BLMyeloid CellsNeutrophilsPneumonia, PneumococcalRecombinant ProteinsStreptococcus pneumoniaeChemokine CXCL2Interferon Type IMembrane ProteinsRecombinant ProteinsSECTM1A protein, mouseCXCL2lung epitheliumneutrophil activationpneumococcal pneumoniatype I IFNs

Identifiers

PMID27064756
PMCPMC5023025
OpenAlexW2325719910

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.