Evidence map›Paper›PMID 22298528›Full record

ArticleAmerican journal of respiratory cell and molecular biology2012

Antiinflammatory role of MUC1 mucin during infection with nontypeable Haemophilus influenzae.

Yoshiyuki Kyo, Kosuke Kato, Yong Sung Park, Sachin Gajghate, Sachin Gajhate, Tsuyoshi Umehara, Erik P Lillehoj, Harumi Suzaki, Kwang Chul Kim

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. MUC1 in the upper-lower airway inflammatory continuum: an endotype-centered perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Innate immune responses in pneumonia.Pneumonia (Nathan Qld.) · 2023
    Review
  9. The role of mucin 1 in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2021
    Review
  10. Review
  11. Article
  12. Review
  13. Non-TypeableInternational journal of molecular sciences · 2020
    Article
  14. MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.American journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

  • Erratum issued
    Gajhate, Sachin [corrected to Gajghate, Sachin]
5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Yoshiyuki KyoDepartment of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Kosuke Kato
Yong Sung Park
Sachin Gajghate
Sachin Gajhate
Tsuyoshi Umehara
Erik P Lillehoj
Harumi Suzaki
Kwang Chul Kim
Temple University · USShowa University · JPUniversity of Maryland, Baltimore · US

Funding

SIGNALING MECHANISM OF MUC1 MUCINR01HL047125 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI KIM, KWANG CHUL · 1991 to 2015
$4.5M
NHLBI NIH HHS R01 HL047125NHLBI NIH HHS R01 HL-47125
6 · The paper itself

Abstract

MUC1 (or Muc1 in nonhuman species) is a membrane-tethered mucin expressed on the apical surface of mucosal epithelia (including those of the airways) that suppresses Toll-like receptor (TLR) signaling. We sought to determine whether the anti-inflammatory effect of MUC1 is operative during infection with nontypeable Haemophilus influenzae (NTHi), and if so, which TLR pathway was affected. Our results showed that: (1) a lysate of NTHi increased the early release of IL-8 and later production of MUC1 protein by A549 cells in dose-dependent and time-dependent manners, compared with vehicle control; (2) both effects were attenuated after transfection of the cells with a TLR2-targeting small interfering (si) RNA, compared with a control siRNA; (3) the NTHi-induced release of IL-8 was suppressed by an overexpression of MUC1, and was enhanced by the knockdown of MUC1; (4) the TNF-α released after treatment with NTHi was sufficient to up-regulate MUC1, which was completely inhibited by pretreatment with a soluble TNF-α receptor; and (5) primary murine tracheal surface epithelial (MTSE) cells from Muc1 knockout mice exhibited an increased in vitro production of NTHi-stimulated keratinocyte chemoattractant compared with MTSE cells from Muc1-expressing animals. These results suggest a hypothetical feedback loop model whereby NTHi activates TLRs (mainly TLR2) in airway epithelial cells, leading to the increased production of TNF-α and IL-8, which subsequently up-regulate the expression of MUC1, resulting in suppressed TLR signaling and decreased production of IL-8. This report is the first, to the best of our knowledge, demonstrating that the inflammatory response in airway epithelial cells during infection with NTHi is controlled by MUC1 mucin, mainly through the suppression of TLR2 signaling.

Indexed as

Base SequenceCytokinesDNA PrimersGene Knockdown TechniquesHaemophilus influenzaeHumansInflammationMucin-1CytokinesDNA PrimersMUC1 protein, humanMucin-1

Identifiers

PMID22298528
PMCPMC3297171
OpenAlexW2040972718

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.