Evidence map›Paper›PMID 31660581›Full record

ArticleClinical and experimental immunology2020

Secretory IgA accumulated in the airspaces of idiopathic pulmonary fibrosis and promoted VEGF, TGF-β and IL-8 production by A549 cells.

K Kobayashi, M Suzukawa, K Watanabe, S Arakawa, S Igarashi, I Asari, A Hebisawa, H Matsui, H Nagai, T Nagase and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. SIgA in various pulmonary diseases.European journal of medical research · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. 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

11 authors at 5 institutions in 1 country.

K KobayashiClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.ORCID 0000-0003-4232-6204
M SuzukawaClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.ORCID 0000-0002-2265-1950
K WatanabeClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
S ArakawaDepartment of Respiratory Medicine, University of Tokyo, Tokyo, Japan.
S IgarashiClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
I AsariClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
A HebisawaClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
H MatsuiClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
H NagaiClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
T NagaseDepartment of Respiratory Medicine, University of Tokyo, Tokyo, Japan.
K OhtaClinical Research Center, National Hospital Organization Tokyo National Hospital, Tokyo, Japan.
Tokyo National Hospital · JPAsahi General Hospital · JPJapan Anti Tuberculosis Association · JPNational Cancer Center Hospital East · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Secretory IgA (SIgA) is a well-known mucosal-surface molecule in first-line defense against extrinsic pathogens and antigens. Its immunomodulatory and pathological roles have also been emphasized, but it is unclear whether it plays a pathological role in lung diseases. In the present study, we aimed to determine the distribution of IgA in idiopathic pulmonary fibrosis (IPF) lungs and whether IgA affects the functions of airway epithelial cells. We performed immunohistochemical analysis of lung sections from patients with IPF and found that mucus accumulated in the airspaces adjacent to the hyperplastic epithelia contained abundant SIgA. This was not true in the lungs of non-IPF subjects. An in-vitro assay revealed that SIgA bound to the surface of A549 cells and significantly promoted production of vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-β and interleukin (IL)-8, important cytokines in the pathogenesis of IPF. Among the known receptors for IgA, A549 cells expressed high levels of transferrin receptor (TfR)/CD71. Transfection experiments with siRNA targeted against TfR/CD71 followed by stimulation with SIgA suggested that TfR/CD71 may be at least partially involved in the SIgA-induced cytokine production by A549 cells. These phenomena were specific for SIgA, distinct from IgG. SIgA may modulate the progression of IPF by enhancing synthesis of VEGF, TGF-β and IL-8.

Indexed as

A549 CellsAgedAged, 80 and overAntigens, CDEpithelial CellsFemaleGene Expression Regulation, NeoplasticHumansIdiopathic Pulmonary FibrosisImmunoglobulin A, SecretoryInterleukin-8LungMaleMiddle AgedReceptors, TransferrinRNA InterferenceAntigens, CDCD71 antigenImmunoglobulin A, SecretoryInterleukin-8Receptors, TransferrinTransforming Growth Factor betaVascular Endothelial Growth Factor Afibrosishumanlungsecretory IgA

Identifiers

PMID31660581
PMCPMC7008227
OpenAlexW2982406718

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.