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Am J Respir Cell Mol Biol ; 53(5): 601-6, 2015 Nov.
Article in English | MEDLINE | ID: mdl-26266960

ABSTRACT

We report that S100 proteins were reduced in patients with chronic rhinosinusitis (CRS). S100A8/9, which is important in epithelial barrier function, was particularly decreased in elderly patients with CRS. Epithelial expression of S100A8/9 is partly regulated by the IL-6 trans-signaling pathway. The goal of this study was to investigate whether or not age-related reduction of S100A8/9 in CRS is associated with blunting of IL-6 trans-signaling. The levels of IL-6, soluble IL-6 receptor (sIL-6R), soluble gp130 (sgp130), and S100A8/9 from control subjects (n = 10), and patients with CRS without nasal polyps (n = 13) and those with CRS with nasal polyps (CRSwNP) (n = 14), were measured by ELISA. Age-related differences in the level of each protein were investigated. Normal human bronchial epithelial cells were cultured in air-liquid interface and stimulated with IL-6/sIL-6R and tumor necrosis factor (TNF)-α with or without the addition of sgp130, a natural inhibitor of IL-6 trans-signaling. There was a significant age-related decline in S100A8/9 and an increase in sgp130 in nasal tissue samples from patients with CRSwNP, although there was no age-related difference in IL-6/sIL-6R production. Additionally, expression of the S100A8/9 gene and protein was increased significantly by IL-6/sIL-6R plus TNF-α in normal human bronchial epithelial cells. This increase was blocked by sgp130. These results suggest that increased sgp130 in older patients may inhibit IL-6 trans-signaling, impair barrier function, and decrease S1008/9 production in elderly patients with CRSwNP. Restoration of barrier function by targeting sgp130 may be a novel treatment strategy.


Subject(s)
Asthma/immunology , Cytokine Receptor gp130/immunology , Interleukin-6/immunology , Nasal Polyps/immunology , Rhinitis/immunology , Sinusitis/immunology , Adult , Age Factors , Aged , Asthma/complications , Asthma/genetics , Asthma/pathology , Bronchi/drug effects , Bronchi/immunology , Bronchi/pathology , Calgranulin A/agonists , Calgranulin A/genetics , Calgranulin A/immunology , Calgranulin B/genetics , Calgranulin B/immunology , Case-Control Studies , Cells, Cultured , Chronic Disease , Cytokine Receptor gp130/genetics , Cytokine Receptor gp130/pharmacology , Epithelial Cells/drug effects , Epithelial Cells/immunology , Epithelial Cells/pathology , Female , Gene Expression Regulation , Humans , Interleukin-6/antagonists & inhibitors , Interleukin-6/genetics , Interleukin-6/pharmacology , Male , Middle Aged , Nasal Polyps/complications , Nasal Polyps/genetics , Nasal Polyps/pathology , Receptors, Interleukin-6/antagonists & inhibitors , Receptors, Interleukin-6/genetics , Receptors, Interleukin-6/immunology , Rhinitis/complications , Rhinitis/genetics , Rhinitis/pathology , Signal Transduction , Sinusitis/complications , Sinusitis/genetics , Sinusitis/pathology , Tumor Necrosis Factor-alpha/genetics , Tumor Necrosis Factor-alpha/immunology , Tumor Necrosis Factor-alpha/pharmacology
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