Evidence map›Paper›PMID 23524653›Full record

ArticleCellular & molecular immunology2013

NOD-like receptors mediated activation of eosinophils interacting with bronchial epithelial cells: a link between innate immunity and allergic asthma.

Chun Kwok Wong, Shuiqing Hu, Karen Ming-Lam Leung, Jie Dong, Lan He, Yi Jun Chu, Ida Miu-Ting Chu, Huai-Na Qiu, Kelly Yan-Ping Liu, Christopher Wai-Kei Lam

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. NOD2-NLRP3 Axis and Asthma.Journal of asthma and allergy · 2025
    Review
  5. Article
  6. Eosinophil-Epithelial Cell Interactions in Asthma.International archives of allergy and immunology · 2024
    Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. NOD-like receptors in asthma.Frontiers in immunology · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Eosinophils: Nemeses of Pulmonary Pathogens?Current allergy and asthma reports · 2019
    Review
  19. 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

10 authors at 3 institutions in 2 countries.

Chun Kwok WongDepartment of Chemical Pathology, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong, China. ck-wong@cuhk.edu.hk
Shuiqing Hu
Karen Ming-Lam Leung
Jie Dong
Lan He
Yi Jun Chu
Ida Miu-Ting Chu
Huai-Na Qiu
Kelly Yan-Ping Liu
Christopher Wai-Kei Lam
Chinese University of Hong Kong · CNPrince of Wales Hospital · CNMacau University of Science and Technology · MO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Key intracytosolic pattern recognition receptors of innate immunity against bacterial infections are nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). We elucidated the NOD1 and NOD2-mediated activation of human eosinophils, the principal effector cells for allergic inflammation, upon interacting with human bronchial epithelial BEAS-2B cells in allergic asthma. Eosinophils constitutively expressed NOD1,2 but exhibited nonsignificant responses to release chemokines upon the stimulation by NOD1 ligand γ-D-glutamyl-meso-diaminopimelic acid (iE-DAP) and NOD2 ligand muramyl dipeptide (MDP). However, iE-DAP and MDP could significantly upregulate cell surface expression of CD18 and intercellular adhesion molecule (ICAM)-1 on eosinophils and ICAM-1 on BEAS-2B cells, as well as induce chemokines CCL2 and CXCL8 release in the coculture system (all P<0.05). Both eosinophils and BEAS-2B cells were the main source for CXCL8 and CCL2 release in the coculture system upon iE-DAP or MDP stimulation. Direct interaction between eosinophils and BEAS-2B cells is responsible for CCL2 release, and soluble mediators are implicated in CXCL8 release. ERK and NF-κB play regulatory roles for the expression of adhesion molecules and chemokines in coculture. Treatment with NOD1,2 ligand could induce the subepithelial fibrosis and significantly enhance the serum concentration of total IgE, chemokine CCL5 for eosinophils and T helper type 2 (Th2) cells and asthma Th2 cytokine IL-13 in bronchoalveolar lavage fluid of ovalbumin-sensitized allergic asthmatic mice (all P<0.05). This study provides further evidence of bacterial infection-mediated activation of NOD1,2 in triggering allergic asthma via the activation of eosinophils interacting with bronchial epithelial cells at inflammatory airway.

Indexed as

Acetylmuramyl-Alanyl-IsoglutamineAnimalsAsthmaBronchiCD18 AntigensCell CommunicationCell LineChemokinesCoculture TechniquesDiaminopimelic AcidEosinophilsExtracellular Signal-Regulated MAP KinasesFemaleHumansImmunity, InnateIntercellular Adhesion Molecule-1Acetylmuramyl-Alanyl-IsoglutamineCD18 AntigensChemokinesDiaminopimelic AcidExtracellular Signal-Regulated MAP KinasesIntercellular Adhesion Molecule-1Interleukin-13N(2)-(gamma-D-glutamyl)-meso-2,2'-diaminopimelic acidNF-kappa BNOD1 protein, humanNod1 Signaling Adaptor ProteinNOD2 protein, humanNod2 Signaling Adaptor Protein

Identifiers

PMID23524653
PMCPMC4003204
OpenAlexW1981970051

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.