Evidence map›Paper›PMID 19965981›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2010

Intelectin is required for IL-13-induced monocyte chemotactic protein-1 and -3 expression in lung epithelial cells and promotes allergic airway inflammation.

Naibing Gu, Guannan Kang, Chang'E Jin, Yongjian Xu, Zhenxiang Zhang, David J Erle, Guohua Zhen

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. The Role of Peptides in Asthma-Obesity Phenotype.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. A 'tad' of hope in the fight against airway disease.Biochemical Society transactions · 2020
    Review
  11. Article
  12. Omentin-A Novel Adipokine in Respiratory Diseases.International journal of molecular sciences · 2017
    Review
  13. Article
  14. Expression of intelectin-1 in bronchial epithelial cells of asthma is correlated with T-helper 2 (Type-2) related parameters and its function.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2017
    Article
  15. Article
  16. Secreted phosphoprotein 1 is a determinant of lung function development in mice.American journal of respiratory cell and molecular biology · 2014
    Article
  17. Article
  18. Article
  19. Inhibitory effect of dexamethasone on expression of cysteine-rich 61 protein in airway epithelial cells of allergic mouse models.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2013
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Naibing GuDivision of Respiratory Diseases, Department of Internal Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Guannan Kang
Chang'E Jin
Yongjian Xu
Zhenxiang Zhang
David J Erle
Guohua Zhen
Huazhong University of Science and Technology · CNTongji Hospital · CNUniversity of California, San Francisco · US

Funding

Airway Epithelial Responses to Allergic InflammationR01HL085089 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ERLE, DAVID J · 2006 to 2010
$1.9M
NHLBI NIH HHS 5R01-HL-085089
6 · The paper itself

Abstract

Asthma is characterized by airway inflammation, mucus overproduction, airway hyperreactivity, and peribronchial fibrosis. Intelectin has been shown to be increased in airway epithelium of asthmatics. However, the role of intelectin in the pathogenesis of asthma is unknown. Airway epithelial cells can secrete chemokines such as monocyte chemotactic protein (MCP)-1 and -3 that play crucial roles in asthmatic airway inflammation. We hypothesized that intelectin plays a role in allergic airway inflammation by regulating chemokine expression. In a mouse allergic asthma model, we found that mRNA expression of intelectin-2 as well as MCP-1 and -3 in mouse lung was increased very early (within 2 h) after allergen challenge. Expression of intelectin protein was localized to mucous cells in airway epithelium. Treatment of MLE12 mouse lung epithelial cells with interleukin IL-13, a critical mediator of allergic airway disease, induced expression of intelectin-1 and -2 as well as MCP-1 and -3. When IL-13-induced intelectin-1 and -2 expression was inhibited by RNA interference, IL-13-induced extracellular signal-regulated kinase 1/2 phosphorylation and MCP-1 and -3 production by MLE12 cells was inhibited. Furthermore, inhibition of intelectin expression by airway transfection with shRNA targeting intelectin-1 and -2 attenuated allergen-induced airway inflammation. We conclude that intelectin, a molecule expressed by airway epithelial cells and upregulated in asthma, is required for IL-13-induced MCP-1 and -3 production in mouse lung epithelial cells and contributes to allergic airway inflammation.

Indexed as

AllergensAnimalsChemokine CCL2Chemokine CCL7Enzyme ActivationEpithelial CellsHypersensitivityInterleukin-13KineticsLectinsLungMiceMitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 6Mucous MembraneOvalbuminAllergensChemokine CCL2Chemokine CCL7Interleukin-13Itlnb protein, mouseLectinsMitogen-Activated Protein Kinase 3Mitogen-Activated Protein Kinase 6Ovalbumin

Identifiers

PMID19965981
PMCPMC2838671
OpenAlexW2101389119

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.