|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
COPD patients had higher interleukin (IL)-1 and IL-8 mRNA expression levels, and these inflammatory cytokines positively correlate with MDA-5 levels.
|
24992168 |
2016 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
COPD airway epithelial cells showed attenuated IL-8 responses to TLR2 agonist despite expressing TLR2 similar to normal, indicating dysregulation in TLR2 signaling pathway.
|
31548332 |
2019 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
IL-8 mRNA levels were significantly higher in COPD patients than in healthy controls (p<0.05), while IL-1β mRNA levels did not differ significantly among the groups.
|
23000304 |
2012 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
IL-8-dependent inflammation is a hallmark of host lung innate immunity to bacterial pathogens, yet in many human lung diseases, including chronic obstructive pulmonary disease, bronchiectasis, and pulmonary fibrosis, there are progressive, irreversible, pathological changes associated with elevated levels of IL-8 in the lung.
|
29894204 |
2018 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
After 18 h of cell culture the basal release of MMP-9 was 2.5-fold, p < 0.02 greater, whereas IL-8 was 1.8-fold (p < 0.01) lower from COPD patient monocytes than from controls.
|
14624669 |
2003 |
|
Chronic Obstructive Airway Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Although IL-8 plays an important role in the chemotaxis of inflammatory cells, the polymorphisms investigated here do not seem to be involved in the genetic predisposition to COPD.
|
16007706 |
2005 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Both miR-34c-5p agomir and CCL22 shRNA could reduce breathing frequency (f), airway resistance (RI), and the levels of IL-8 and TNF-α in BALF of COPD rats with increased Cydn (dynamic lung compliance) and PIF (peak inspiratory flow).
|
31032652 |
2020 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
BRD4 is increased in the lung of patients with COPD and is correlated with miR-29b and IL-8 expression. miR-29b regulates cigarette smoke extract (CSE)-induced IL-8 expression by targeting BRD4 in HBE cells.
|
30652495 |
2019 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Cigarette smoke dose-dependently induced apoptosis, proliferation and CXCL8 release with normal epithelial cells being more responsive than COPD patient derived cells.
|
28468623 |
2017 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
LHGDN |
Cigarette smoke is the leading risk factor for the development of chronic obstructive pulmonary disease (COPD) an inflammatory condition characterised by neutrophilic inflammation and release of proinflammatory mediators such as interleukin-8 (IL-8).
|
16029496 |
2005 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
COPD cell cultures displayed reduced antibacterial activity, whereas smoke exposure suppressed the NTHi-induced expression of AMPs and further increased IL-8 expression in COPD and non-COPD cultures.
|
28171878 |
2017 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Corticosteroid sensitivity was determined as the 50% inhibitory concentration of dexamethasone on tumor necrosis factor-α-induced interleukin-8 release in peripheral blood mononuclear cells from patients with COPD (n = 17) and compared with that of nonsmoking (n = 8) and smoking (n = 7) control subjects.
|
20224070 |
2010 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
CSE alone elevated cytokine secretion in all examined cells. rhHsp70 and CSE had antagonistic interactions on IL-8 release in PBECs from COPD patients, while the addition of rhHsp70 further increased CSE-induced IL-6 secretion in NHBE cells. rhHsp70 and CSE alone decreased TLR2 and TLR4 mRNA expression in COPD-derived PBECs.
|
30268700 |
2019 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
CTD_human |
Decreased FoxO3A in COPD cells was associated with increased phosphorylation of EGFR, Akt and FoxO3A and treatment with quercetin, LY294002 or erlotinib increased nuclear FoxO3A and decreased IL-8 and phosphorylation of Akt, EGFR and FoxO3A, Compared with control, elastase/LPS-exposed mice showed decreased nuclear FoxO3A, increased chemokines and phosphorylation of EGFR and Akt.
|
23099361 |
2013 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
DHBE cells exhibit a dampened IL-8 release, indicating that COPD is associated with a reduced capacity of airway epithelial cells to respond to foreign material.
|
23499888 |
2013 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
ELISA assay showed hydrogen-rich saline lowered the levels of pro-inflammatory cytokines (IL-8 and IL-6) and anti-inflammatory cytokine IL-10 in bronchoalveolar lavage fluid and serum of chronic obstructive pulmonary disease rats.
|
28795606 |
2017 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Fluticasone propionate (FP) and dexamethasone (DEX) suppressed IL-6 and IL-8 production in BEAS-2B cells, but clarithromycin (CAM) failed to do so.<b>Conclusions:</b><i>P. aeruginosa</i>-derived flagellin-induced IL-6 and IL-8 production in bronchial epithelial cells, which partially explains the mechanisms of progression and exacerbation of COPD.
|
31517562 |
2019 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
For IL-8 and GM-CSF efficiency of dexamethasone was NS > S > COPD.
|
20801891 |
2010 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
For inflammatory cytokines, lncRNA ANRIL expression was negatively correlated with TNF-α (P < 0.001), IL-1β (P = 0.015), IL-8 (P = 0.008), IL-17A (P = 0.002), and LTB-4 (P = 0.004) in AECOPD patients, while it was negatively correlated with TNF-α (P = 0.049), IL-1β (P = 0.005), IL-17A (P = 0.030), and LTB-4 (P = 0.011) in stable COPD patients.
|
30230590 |
2019 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
Furthermore, IL-8 has been shown to be a pro-inflammatory marker in bronchiectasis, COPD and allergic asthma.
|
30380761 |
2018 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Gene expression analysis showed that CSE suppressed LPS-induced TNF-α transcription but not CXCL8 transcription in COPD alveolar macrophages.
|
24528166 |
2014 |
|
Chronic Obstructive Airway Disease
|
0.400 |
Biomarker
|
disease |
BEFREE |
However, following active filtration, we only observed significant reductions on systemic inflammation measured as of IL-8 at 58.59% (95% CI: -76.31, -27.64) in the total group of participants and 70.04% (95% CI: -83.05, -47.05) in the subset of COPD patients, with adjustments.
|
28645052 |
2017 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
IL-10 disrupts the Brd4-docking sites to inhibit LPS-induced CXCL8 and TNF-α expression in monocytes: Implications for chronic obstructive pulmonary disease.
|
26044852 |
2015 |
|
Chronic Obstructive Airway Disease
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
In COPD PHLFs, the induction of miR-146a-5p was significantly less compared with controls and was associated with the SNP rs2910164 (GG allele) in the miR-146a-5p gene.Our results suggest that induction of miR-146a-5p is involved in epithelial-fibroblast communication in the lungs and negatively regulates epithelial-derived IL-1α induction of IL-8 by fibroblasts.
|
28546273 |
2017 |
|
Chronic Obstructive Airway Disease
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In addition, mediators that are regulated by the A(2B)R, such as IL-6, IL-8 and osteopontin were elevated in these samples and activation of the A(2B)R on cells isolated from the airways of COPD and IPF patients was shown to directly induce the production of these mediators.
|
20169073 |
2010 |