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Cited by 262Asthma and respiratory diseasesChemokine receptors and signalingAllergic Rhinitis and Sensitization

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

Airway Epithelial Cells Release MIP-3α/CCL20 in Response to Cytokines and Ambient Particulate Matter

Reibman, Joan, Hsu, Yanshen, Chen, Lung Chi, Bleck, Bertram, Gordon, Terry·2003·American Journal of Respiratory Cell and Molecular Biology
DOI 10.1165/rcmb.2002-0095oc
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Abstract

The initiation and maintenance of airway immune responses in Th2 type allergic diseases such as asthma are dependent on the specific activation of local airway dendritic cells (DCs). The cytokine microenvironment, produced by local cells, influences the recruitment of specific subsets of immature DCs and their subsequent maturation. In the airway, DCs reside in close proximity to airway epithelial cells (AECs). We examined the ability of primary culture human bronchial epithelial cells (HBECs) to synthesize and secrete the recently described CC-chemokine, MIP-3α/CCL20. MIP-3α/CCL20 is the unique chemokine ligand for CCR6, a receptor with a restricted distribution. MIP-3α/CCL20 induces selective migration of DCs because CCR6 is expressed on some immature DCs but not on CD14+ DC precursors or mature DCs. HBECs were stimulated with pro-inflammatory cytokines tumor necrosis factor-α and interleukin (IL)-1β or, because of their critical role in allergic diseases, IL-4 and IL-13. Cells were also exposed to small size-fractions of ambient particulate matter. Each of these stimuli induced MIP-3α/CCL20 gene and protein expression. Moreover, these agents upregulated mitogen-activated protein kinase pathways in HBECs. Inhibition of the ERK1/2 pathway or p38 reduced cytokine-induced MIP-3α/CCL20 expression. These data suggest a mechanism by which AEC may facilitate recruitment of DC subsets to the airway.

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Crossref · 10.1165/rcmb.2002-0095oc

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Research works printed but not linked: 3

  1. 2001, Curr. Opin. Allergy Clin. Immunol., 1, 51, 10.1097/00130832-200102000-00010 · DOI
  2. 2002, Transplantation, 73(1 Suppl), S7
  3. 1997, Blood, 89, 3315

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Metadata

Authors
Reibman, J., Hsu, Y., Chen, L. C., Bleck, B., & Gordon, T.
Affiliations
New York University (US)
Corresponding author
Reibman, Joan
ORCID
Venue
American Journal of Respiratory Cell and Molecular Biology
Publisher
Oxford University Press (OUP)
Published
2003-06-01
Volume
28
Issue
6
Pages
648-654
ISSN
  • 1044-1549 (ISSN-L)
  • 1535-4989
DOI
10.1165/rcmb.2002-0095oc
OpenAlex
W2041791106
Cited by
262
References
44
Citations by year
2026: 4 · 2025: 2 · 2024: 5 · 2023: 3 · 2022: 5 · 2021: 6 · 2020: 6 · 2019: 5 · 2018: 8 · 2017: 8 · 2016: 8 · 2015: 14 · 2014: 20 · 2013: 17 · 2012: 13
FWCI
9.01
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Public Health Service (T3207267)
  • National Institute of Environmental Health Sciences (ES00260, P30ES000260, R01ES010187, ES10187)
  • National Center for Research Resources (M01 RR 00096, M01RR000096)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Asthma and respiratory diseases
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
Keywords
airway epithelial cells, bronchial epithelial cells, dendritic cell recruitment, CCR6, asthma, particulate matter, ERK signaling, p38 MAPK, IL-4, IL-13, TNF-α, IL-1β, airway immune response
MeSH terms
Air Pollutants, Bronchi, Cells, Cultured, Dendritic Cells, Enzyme Inhibitors, Epithelial Cells, Flavonoids, Humans, Imidazoles, Particle Size, Pyridines, RNA, Messenger, Cytokines, Macrophage Inflammatory Proteins, Receptors, Chemokine, Chemokines, CC, Mitogen-Activated Protein Kinase 1, Respiratory Mucosa, Mitogen-Activated Protein Kinases, MAP Kinase Signaling System, Mitogen-Activated Protein Kinase 3, Receptors, CCR6, Chemokine CCL20

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