Consequently, α-LacCer also ameliorated both α-GalCer and GSL-1-induced airway hyperreactivity and α-GalCer-induced neutrophilia when co-administered <i>in vivo</i>.
Pre-treatment with H<sub>2</sub>O<sub>2</sub> did not alter antioxidant responses in COPD bronchial epithelial cells and, more modestly than in asthma, reduced poly(I:C)-induced IFNβ gene expression.
Sputum from subjects with asthma (n = 87) or COPD (n = 73) and ACO (n = 68) or from smokers (n = 62) and never-smokers (n = 62) was analyzed for high mobility group protein B1 (HMGB1), heat shock protein 70 (HSP70), LL-37, S100A8, and galectin-3 (Gal-3).
Sputum from subjects with asthma (n = 87) or COPD (n = 73) and ACO (n = 68) or from smokers (n = 62) and never-smokers (n = 62) was analyzed for high mobility group protein B1 (HMGB1), heat shock protein 70 (HSP70), LL-37, S100A8, and galectin-3 (Gal-3).
Sputum from subjects with asthma (n = 87) or COPD (n = 73) and ACO (n = 68) or from smokers (n = 62) and never-smokers (n = 62) was analyzed for high mobility group protein B1 (HMGB1), heat shock protein 70 (HSP70), LL-37, S100A8, and galectin-3 (Gal-3).
Sputum from subjects with asthma (n = 87) or COPD (n = 73) and ACO (n = 68) or from smokers (n = 62) and never-smokers (n = 62) was analyzed for high mobility group protein B1 (HMGB1), heat shock protein 70 (HSP70), LL-37, S100A8, and galectin-3 (Gal-3).
Our results also show that A20 expression was significantly reduced in blood leukocytes and ASM obtained from patients with asthma compared to cells obtained from healthy subjects which was restored after incubation with IRL201104 in vitro, when added alone, or in combination with LPS or TNF-α in ASM.
Our results also show that A20 expression was significantly reduced in blood leukocytes and ASM obtained from patients with asthma compared to cells obtained from healthy subjects which was restored after incubation with IRL201104 in vitro, when added alone, or in combination with LPS or TNF-α in ASM.
Understanding the mechanisms by which these LncRNAs regulate CF disease phenotype will help develop novel therapeutic targets for CF and related pulmonary diseases, such as COPD and Asthma.
To evaluate the nutritional status of vitD and the frequency of VDR gene polymorphisms, as well as identify their associations with nutritional status and asthma.
Finally, through simultaneous measurement of PBMC proteins on the nCounter assay, we identified CD28 and OX40 (<i>TNFRSF4</i>), both of which are critical co-stimulatory molecules during T-cell activation, as significantly upregulated in asthmatics.
Finally, through simultaneous measurement of PBMC proteins on the nCounter assay, we identified CD28 and OX40 (<i>TNFRSF4</i>), both of which are critical co-stimulatory molecules during T-cell activation, as significantly upregulated in asthmatics.
Mucins are glycoproteins that are mainly responsible for the viscoelastic property of mucus, and MUC5AC is a major mucin glycoprotein that is overproduced in asthma.
The expression of HMGB1 could be negatively regulated by HSF1, and the TLR4/MyD88/NF-κB signal pathway was involved in HSF1/HMGB1-mediated regulation of asthma.
The expression of HMGB1 could be negatively regulated by HSF1, and the TLR4/MyD88/NF-κB signal pathway was involved in HSF1/HMGB1-mediated regulation of asthma.