Evidence map›Paper›PMID 30570135›Full record

ReviewClinical and experimental immunology2019

Secretory immunoglobulin A induces human lung fibroblasts to produce inflammatory cytokines and undergo activation.

S Arakawa, M Suzukawa, K Watanabe, K Kobayashi, H Matsui, H Nagai, T Nagase, K Ohta

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. SIgA in various pulmonary diseases.European journal of medical research · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Impaired salivary SIgA antibodies elicit oral dysbiosis and subsequent induction of alveolar bone loss.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    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 2 institutions in 1 country.

S ArakawaNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
M SuzukawaNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
K WatanabeNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
K KobayashiNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
H MatsuiNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
H NagaiNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
T NagaseDepartment of Respiratory Medicine, University of Tokyo, Tokyo, Japan.
K OhtaNational Hospital Organization Tokyo National Hospital, Tokyo, Japan.
Tokyo National Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoglobulin (Ig)A is the most abundant immunoglobulin in humans, and in the airway mucosa secretory IgA (sIgA) plays a pivotal role in first-line defense against invading pathogens and antigens. IgA has been reported to also have pathogenic effects, including possible worsening of the prognosis of idiopathic pulmonary fibrosis (IPF). However, the precise effects of IgA on lung fibroblasts remain unclear, and we aimed to elucidate how IgA activates human lung fibroblasts. We found that sIgA, but not monomeric IgA (mIgA), induced interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1 and granulocyte-macrophage colony-stimulating factor (GM-CSF) production by normal human lung fibroblasts (NHLFs) at both the protein and mRNA levels. sIgA also promoted proliferation of NHLFs and collagen gel contraction comparable to with transforming growth factor (TGF)-β, which is involved in fibrogenesis in IPF. Also, Western blot analysis and real-time quantitative polymerase chain reaction (PCR) revealed that sIgA enhanced production of α-smooth muscle actin (α-SMA) and collagen type I (Col I) by NHLFs. Flow cytometry showed that NHLFs bound sIgA, and among the known IgA receptors, NHLFs significantly expressed CD71 (transferrin receptor). Transfection of siRNA targeting CD71 partially but significantly suppressed cytokine production by NHLFs co-cultured with sIgA. Our findings suggest that sIgA may promote human lung inflammation and fibrosis by enhancing production of inflammatory or fibrogenic cytokines as well as extracellular matrix, inducing fibroblast differentiation into myofibroblasts and promoting human lung fibroblast proliferation. sIgA's enhancement of cytokine production may be due partially to its binding to CD71 or the secretory component.

Indexed as

ActinsAntigens, CDCells, CulturedCytokinesFibroblastsHumansIdiopathic Pulmonary FibrosisImmunoglobulin A, SecretoryLungReceptors, TransferrinACTA2 protein, humanActinsAntigens, CDCD71 antigenCytokinesImmunoglobulin A, SecretoryReceptors, TransferrinfibroblastsfibrosishumanIgAlung

Identifiers

PMID30570135
PMCPMC6378381
OpenAlexW2906085902

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.