These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regulation of interleukin-33 and thymic stromal lymphopoietin in human nasal fibroblasts by proinflammatory cytokines.
    Author: Nomura K, Kojima T, Fuchimoto J, Obata K, Keira T, Himi T, Sawada N.
    Journal: Laryngoscope; 2012 Jun; 122(6):1185-92. PubMed ID: 22460292.
    Abstract:
    OBJECTIVES/HYPOTHESIS: Epithelial-derived interleukin (IL)-33 and thymic stromal lymphopoietin (TSLP) are critical regulators of innate and adaptive immune responses associated with Th2 cytokine-mediated inflammation, including allergic rhinitis. IL-33 and TSLP are expressed not only in epithelial cells but also fibroblasts, endothelial cells, and smooth muscle cells at nasal mucosal sites. However, the role and the regulation of IL-33 and TSLP in nasal fibroblasts remain unknown. We investigated the signal transduction regulation of IL-33 and TSLP induced by proinflammatory cytokines in nasal fibroblasts. STUDY DESIGN: In vitro, prospective study. METHODS: Nasal fibroblasts were derived from human nasal mucosa without allergic rhinitis. Expression of IL-33 and TSLP was examined in nasal fibroblasts treated with proinflammatory cytokines IL-1β or tumor necrosis factor (TNF)-α after pretreatment with or without various inhibitors of signal transduction pathways. RESULTS: In nasal fibroblasts, both Western blotting and reverse transcriptase-polymerase chain reaction demonstrated that expression of mRNAs and proteins of IL-33 and TSLP was increased by treatment with IL-1β or TNF-α. Immunostaining revealed that IL-33-positive nuclei were markedly increased by the treatment with IL-1β or TNF-α. Enzyme-linked immunosorbent assay showed that fibroblast-released TSLP was significantly increased by treatment with IL-1β or TNF-α. The upregulation of both IL-33 and TSLP proteins by treatment with IL-1β was prevented by inhibitors of pan- protein kinase C (PKC), p38 mitogen-activated protein kinase, and nuclear factor (NF)-κB. In the cells treated with TNF-α, upregulation of IL-33 protein was prevented by inhibitors of phosphoinositide 3-kinase (PI3K), c-Jun N-terminal kinase (JNK), and NF-κB, whereas upregulation of TSLP protein was prevented by inhibitors of pan-PKC, PI3K, JNK, and NF-κB. CONCLUSIONS: Expression of IL-33 and TSLP in nasal fibroblasts was regulated via distinct signal transduction pathways including NF-κB.
    [Abstract] [Full Text] [Related] [New Search]