The TNF-α and IL-1β levels in EBC were significantly higher in the COPD groups compared with the non-COPD group before surgery (all P < 0.01), and the levels were significantly decreased after lung-protective treatment was received before surgery (all P < 0.01).
The aim of the present work was to investigate the association between the Y113H polymorphism (rs1051740) in EPHX1 gene and -308G/A polymorphism (rs1800629) in TNF-a gene and COPD in Kazakhstan population.
Insulin resistance has been associated with cytokines, including interleukin-6 and tumor necrosis factor alpha soluble receptor, both of which are elevated in chronic obstructive pulmonary disease (COPD).
In lung tumors, levels of tumor necrosis factor-α, transforming growth factor-β, and IL-10 were higher than in nontumor parenchyma in the LC-COPD group, whereas IL-2 and vascular endothelial growth factor levels were higher in tumors of both the LC-only and LC-COPD groups.
Increased levels of tumor necrosis factor (TNF) α have been linked to a number of pulmonary inflammatory diseases including asthma, chronic obstructive pulmonary disease (COPD), acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), sarcoidosis, and interstitial pulmonary fibrosis (IPF).
Moreover, as a combination of tumor necrosis factor-α (TNF-α) and TGF-β1 have been shown to have a cumulative impact on the severity of airflow limitation in COPD, the TNF-α release was also measured in a representative subgroup of patients.
The serum mtDNA, IL-6 and IL-10 levels in the control group and in the COPD group increased rapidly at 2 h and peaked at 24 h, while TNF-α levels peaked at 2 h and subsequently decreased.
Tumor necrosis factor-alpha (TNF-α) is a potent pro-inflammatory mediator and its expression is up-regulated in chronic obstructive pulmonary disease (COPD).
Chronic obstructive pulmonary disease (COPD) is characterized by reduced lung function associated with increased local and systemic inflammatory markers, such as TNFα and IL-1β.
Levels of miR-223 are induced by interleukin-1β and tumor necrosis factor-α. miR-223 controls the expression of fractalkine by targeting histone deacetylase 2. miR-223 levels are increased in COPD mouse models. miR-223 levels inversely correlate with HDAC2 expression in COPD patients.
Acupuncture treatment appeared to protect pulmonary function and reduce the COPD-induced inflammatory response by decreasing cell inflammation and the production of TNF-α and IL-8.
The analysis of gene expressions using a qPCR array revealed that many cytokines contributing to the pathogenesis and systemic inflammation in chronic obstructive pulmonary disease (COPD), including CCL2, CCL20, CSF2, CXCL1, CXCL10, IL1B and TNFα, were down-regulated by MA130 but not by a PKCζ-inactive control compound.
IL-10 disrupts the Brd4-docking sites to inhibit LPS-induced CXCL8 and TNF-α expression in monocytes: Implications for chronic obstructive pulmonary disease.
There are genetic variants in the TNF promoter associated with increased risk of COPD secondary to smoking and with a higher GOLD grade in the Mexican Mestizo population.
In addition, it was shown that important determinants of prognosis of COPD such as FEV1, BMI, COPD exacerbation and hospitalization were not associated with TNF-α-308 gene polymorphism.
Moreover, inhibiting Src deterred the cigarette smoke-mediated induction of matrix metalloproteinase-9 and -12 in alveolar macrophages and lung expression of cathepsin K, IL-17, TNF-α, MCP-1, and KC, all key factors in the pathogenesis of COPD.
Inflammatory cell and cytokine profile (nuclear factor-κB, IL-6, tumor necrosis factor-α), intracellular polymerization of Z-AT, and endoplasmic reticulum (ER) stress markers (protein kinase RNA-like ER kinase, activator transcription factor 4) were assessed in transgenic mice and transfected cells in response to cigarette smoke, and in explanted lungs from ZZ and MM individuals with severe COPD.
In the present study, we detected the cytochrome P4501A1 gene (CYP1A1) MspI polymorphism and the tumor necrosis factor alpha (TNFα)-308 single nucleotide polymorphism in COPD patients, and investigated their associations with smoking and COPD susceptibility in Inner Mongolia.
Recently we observed increased adipose tissue (AT) expression of CD40-related signaling proteins but no activation of tumor necrosis factor-α or CD68 in patients with chronic sustained hypoxia resulting from chronic obstructive pulmonary disease (COPD).