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Club Cell Protein-16 modifies airway inflammation in asthma and is associated with significant clinical asthma outcomes
Conclusion: Lack of CC16 results in enhanced T2 inflammatory responses in both human primary cell culture and a mouse model. CC16 mRNA levels inversely correlated with MUC5AC which was supported by the CC16 knockdown experiments, and significantly associated with clinically relevant asthma outcomes.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Kraft, M., Ledford, J., Gozdz, J., Li, X., Francisco, D., Manne, A., Guerra, S., Martinez, F., Kaminski, N., Wenzel, S., Meyers, D., Bleecker, E. Tags: Clinical Problems Source Type: research

MUC1-CT mediates corticosteroid responses in COPD
Conclusions: MUC1-CT mediates the anti-inflammatory properties of corticosteroids and the lack of its expression in COPD increases resistance to corticosteroids.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Diaz, L., Milara, J., Morcillo, E., Serrano, A., Guijarro, R., Sanz, C., Cortijo, J. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research

LATE-BREAKING ABSTRACT: MUC1 downregulation induces corticosteroid resistance in asthma's in vitro and in vivo models
Conclusion: MUC1 downregulation may lack the anti-inflammatory effects of corticosteroids in Asthma.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Morell, A., Bel, E., Milara, J., Morcillo, E., Cortijo, J. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research

Role of protein phosphatase 5 (PP5) in mediating corticosteroid insensitivity in airway smooth muscle (ASM) cells in severe asthma
Although the mechanisms mediating corticosteroid resistance in severe asthma are still unknown, recent evidence suggests ASM cells isolated from patients with severe asthma have a decreased insensitivity to dexamethasone (Dex) with respect to the inhibition of chemokine production. Here we investigated whether this corticosteroid insensitivity seen in ASM from severe asthmatics was due to an abnormal GR signalling pathway. We here observed that production of CCL5 and CCL11 by TNF in ASM cells from severe asthmatics (compared to healthy subjects and nonsevere asthma) was not affected by Dex or fluticasone (FP) pretreatment....
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Chachi, L., Abbasian, M., Gavrila, A., Tliba, O., Brightling, C., Amrani, Y. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

LATE-BREAKING ABSTRACT: Inhibition of the ubiquitin-E3-ligase FBXW7 enhances steroid efficacy: New concept for treating steroid insensitivity
Conclusion: Reduction of FBXW7 caused a significant augmentation of functional GR and may have the potential to improve the efficacy of steroids.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Kaestle, M., Wyatt, D., Nicklin, P. Tags: 5.3 Allergy and Immunology Source Type: research

Protein tyrosine phosphatase PTPRR regulates PP2A in mononuclear cells
Conclusion: We have demonstrated that reduction of PTPRR down-regulates PP2AC via enhancement of PP2AC-Tyr307 phosphorylation that may lead to corticosteroid insensitivity. This novel mechanism may be a new therapeutic target for restoration of corticosteroid sensitivity in patients with severe asthma.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Kobayashi, Y., Miller-Larsson, A., Ito, K., Kanda, A., Tomoda, K., Barnes, P. J., Mercado, N. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research