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Respiratory syncytial virus induces functional thymic stromal lymphopoietin receptor in airway epithelial cells.
J Inflamm Res 2013; 6:53-61JI

Abstract

The epithelial-derived cytokine thymic stromal lymphopoietin (TSLP) plays a key role in the development and progression of atopic disease and has notably been shown to directly promote the allergic inflammatory responses that characterize asthma. Current models suggest that TSLP is produced by epithelial cells in response to inflammatory stimuli and acts primarily upon dendritic cells to effect a T helper type 2-type inflammatory response. Recent reports, however, have shown that epithelial cells themselves are capable of expressing the TSLP receptor (TSLPR), and may thus directly contribute to a TSLP-dependent response. We report here that beyond simply expressing the receptor, epithelial cells are capable of dynamically regulating TSLPR in response to the same inflammatory cues that drive the production of TSLP, and that epithelial cells produce chemokine C-C motif ligand 17, a T helper type 2-associated chemokine, in response to stimulation with TSLP. These data suggest that a direct autocrine or paracrine response to TSLP by epithelial cells may initiate the initial waves of chemotaxis during an allergic inflammatory response. Intriguingly, we find that the regulation of TSLPR, unlike TSLP, is independent of nuclear factor kappa-light-chain-enhancer of activated B cells, suggesting that the cell may be able to independently regulate TSLP and TSLPR levels in order to properly modulate its response to TSLP. Finally, we show evidence for this dynamic regulation occurring following the viral infection of primary epithelial cells from asthmatic patients. Taken together, the data suggest that induction of TSLPR and a direct response to TSLP by epithelial cells may play a novel role in the development of allergic inflammation.

Authors+Show Affiliations

Immunology Program, Benaroya Research Institute, Seattle, WA ; Department of Immunology, University of Washington School of Medicine, Seattle, WA.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23576878

Citation

Miazgowicz, Michael M., et al. "Respiratory Syncytial Virus Induces Functional Thymic Stromal Lymphopoietin Receptor in Airway Epithelial Cells." Journal of Inflammation Research, vol. 6, 2013, pp. 53-61.
Miazgowicz MM, Elliott MS, Debley JS, et al. Respiratory syncytial virus induces functional thymic stromal lymphopoietin receptor in airway epithelial cells. J Inflamm Res. 2013;6:53-61.
Miazgowicz, M. M., Elliott, M. S., Debley, J. S., & Ziegler, S. F. (2013). Respiratory syncytial virus induces functional thymic stromal lymphopoietin receptor in airway epithelial cells. Journal of Inflammation Research, 6, pp. 53-61. doi:10.2147/JIR.S42381.
Miazgowicz MM, et al. Respiratory Syncytial Virus Induces Functional Thymic Stromal Lymphopoietin Receptor in Airway Epithelial Cells. J Inflamm Res. 2013;6:53-61. PubMed PMID: 23576878.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Respiratory syncytial virus induces functional thymic stromal lymphopoietin receptor in airway epithelial cells. AU - Miazgowicz,Michael M, AU - Elliott,Molly S, AU - Debley,Jason S, AU - Ziegler,Steven F, Y1 - 2013/03/24/ PY - 2013/4/12/entrez PY - 2013/4/12/pubmed PY - 2013/4/12/medline KW - RSV KW - TSLP KW - TSLPR KW - asthma KW - epithelium SP - 53 EP - 61 JF - Journal of inflammation research JO - J Inflamm Res VL - 6 N2 - The epithelial-derived cytokine thymic stromal lymphopoietin (TSLP) plays a key role in the development and progression of atopic disease and has notably been shown to directly promote the allergic inflammatory responses that characterize asthma. Current models suggest that TSLP is produced by epithelial cells in response to inflammatory stimuli and acts primarily upon dendritic cells to effect a T helper type 2-type inflammatory response. Recent reports, however, have shown that epithelial cells themselves are capable of expressing the TSLP receptor (TSLPR), and may thus directly contribute to a TSLP-dependent response. We report here that beyond simply expressing the receptor, epithelial cells are capable of dynamically regulating TSLPR in response to the same inflammatory cues that drive the production of TSLP, and that epithelial cells produce chemokine C-C motif ligand 17, a T helper type 2-associated chemokine, in response to stimulation with TSLP. These data suggest that a direct autocrine or paracrine response to TSLP by epithelial cells may initiate the initial waves of chemotaxis during an allergic inflammatory response. Intriguingly, we find that the regulation of TSLPR, unlike TSLP, is independent of nuclear factor kappa-light-chain-enhancer of activated B cells, suggesting that the cell may be able to independently regulate TSLP and TSLPR levels in order to properly modulate its response to TSLP. Finally, we show evidence for this dynamic regulation occurring following the viral infection of primary epithelial cells from asthmatic patients. Taken together, the data suggest that induction of TSLPR and a direct response to TSLP by epithelial cells may play a novel role in the development of allergic inflammation. SN - 1178-7031 UR - https://www.unboundmedicine.com/medline/citation/23576878/Respiratory_syncytial_virus_induces_functional_thymic_stromal_lymphopoietin_receptor_in_airway_epithelial_cells_ L2 - https://dx.doi.org/10.2147/JIR.S42381 DB - PRIME DP - Unbound Medicine ER -