Association of Tumor Necrosis Factor-α Gene Promoter Polymorphism With Low Attenuation Areas on High-Resolution CT in Patients With COPD

Sakao, Seiichiro; Igari, Hidetoshi; Watanabe, Reiko; Shino, Yuji; Shirasawa, Hiroshi; Kuriyama, Takayuki

doi:10.1378/chest.122.2.416

Cited by 82 publications

(47 citation statements)

References 25 publications

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“…A TNF-α gene polymorphism resulting in increased TNF-α levels has also been described in a population that is uniquely susceptible to the development of COPD (Huang et al 1997;Sakao et al 2002), although other studies have not been able to corroborate this fi nding (Higham et al 2000;Ferrarotti et al 2003). Interestingly, serum concentrations of TNF-α, as well as TNF-α secretion by monocytes, is particularly robust in the subset of COPD patients with weight loss or cachexia (Di Francia et al 1994;De Godoy et al 1996;Pitsiou et al 2002).…”

Section: Tumor Necrosis Factor-alpha (Tnf-α)mentioning

confidence: 99%

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Gadgil

Duncan

2008

COPD

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Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the US and a major worldwide healthcare problem. The pathophysiologic mechanisms that drive development and progression of this disease are complex and only poorly understood. While tobacco smoking is the primary risk factor, other disease processes also appear to play a role. Components of the innate immune system (eg, macrophages and neutrophils) have long been believed to be important in the development of COPD. More recent evidence also suggests involvement of the adaptive immune system in pathogenesis of this disease. Here we will review the literature supporting the participation of T-cells in the development of COPD, and comment on the potential antigenic stimuli that may account for these responses. We will further explore the prospective contributions of T-cell derived mediators that could contribute to the infl ammation, alveolar wall destruction, and small airway fi brosis of advanced COPD. A better understanding of these complex immune processes will lead to new insights that could result in improved preventative and/or treatment strategies.

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Section: Tumor Necrosis Factor-alpha (Tnf-α)mentioning

confidence: 99%

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Gadgil

Duncan

2008

COPD

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“…TNF-α (-308*A/G) PCR products were digested with restriction endonuclease NcoI (sequence of restriction site: CqCATGG) for 2 hours. DNA-fragments were analyzed on 2-3% agarose gels stained with ethidium bromide (Schulte et al, 2001;Sakao et al, 2002;Shahbazi et al, 2002). …”

Section: Genotypingmentioning

confidence: 99%

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

Shi

Ren²,

Lu³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…TNF-α has been shown to correlate with body mass index (BMI) and cigarette smoke exposure [71,72] and other inflammatory mediators [73] in COPD. A polymorphism of the promoter region of the TNF-α gene has been implicated in the occurrence, severity, and mortality risk of COPD [74][75][76].…”

Section: Role Of Tnf-α In Asthma and Copdmentioning

confidence: 99%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

117

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Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation, has been implicated in several inflammatory conditions. It plays a significant role in many inflammatory diseases of lung. Given that there is significant literature supporting the pathobiologic role of TNF-α in asthma, mainly in severe refractory asthma, and COPD, TNF-α inhibitors (infliximab, golimumab and etanercept) are now regarded as potential new medications in asthma and COPD management. The studies reported in literature indicate that TNF-α inhibitors are effective in a relatively small subgroup of patients with severe asthma, possibly defined by an increased TNF axis, but they seem to be ineffective in COPD, although an observational study demonstrated that TNF-α inhibitors were associated with a reduction in the rate of COPD hospitalisation among patients with COPD receiving these agents to treat their rheumatoid arthritis. These findings require a smart approach because there is still good reason to target TNF-α, perhaps in a more carefully selected patient group. TNF-α treatment should therefore not be thrown out, or abandoned. Indeed, since severe asthma and COPD are heterogeneous diseases that have characteristics that occur with different phenotypes remained poorly characterized and little known about the underlying pathobiology contributing to them, it is likely that definition of these phenotypes and choice of the right outcome measure will allow us to understand which kind of patients can benefit from TNF-α inhibitors.

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Association of Tumor Necrosis Factor-α Gene Promoter Polymorphism With Low Attenuation Areas on High-Resolution CT in Patients With COPD

Cited by 82 publications

References 25 publications

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Role of T-lymphocytes and pro-inflammatory mediators in the pathogenesis of chronic obstructive pulmonary disease

Association Between EGF, TGF-β1 and TNF-α Gene Polymorphisms and Hepatocellular Carcinoma

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

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