Tumor necrosis factor-alpha levels and weight loss in chronic obstructive pulmonary disease.

Francia, M Di; Barbier, Dominique; Mège, Jean Louis; Orehek, J

doi:10.1164/ajrccm.150.5.7952575

Cited by 434 publications

(295 citation statements)

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“…It is line with studies showing relationship between losing weight and serum TNF-α in COPD [8,12,15,37]. Alteration of FEV1 values might not be strictly related to change in airway calibre but may also depend on pulmonary elastolysis and reduced respiratory skeletal muscle forces, both processes likely to be influenced by TNF-α [6,15].…”

Section: Discussionsupporting

confidence: 85%

Local and systemic cellular inflammation and cytokine release in chronic obstructive pulmonary disease

Moermans¹,

Heinen

Nguyen

et al. 2011

Cytokine

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Background: Chronic obstructive pulmonary disease (COPD) is a chronic airway inflammatory disease caused by repeated exposure to noxious gases or particles. It is now recognized that the disease also features systemic inflammation. The purpose of our study was to compare airway and systemic inflammation in COPD to that seen in healthy subjects and to relate the inflammation with the disease severity. Methods: Ninety-five COPD patients, encompassing the whole severity spectrum of the disease, were recruited from our outpatient clinic and rehabilitation center and compared to 33 healthy subjects. Induced sputum and blood samples were obtained for measurement of inflammatory cell count. Interleukin (IL)-4, IL-6, IL-10, TNF-α and IFN-γ produced by 24 h sputum and blood cell cultures were measured. Results: Compared to healthy subjects, COPD exhibited a prominent airway neutrophilic inflammation associated with a marked IL-10, IL-6 and TNF-α release deficiency that contrasted with a raised IFN-γ production. Neutrophilic inflammation was also prominent at blood level together with raised production of IFN-γ, IL-10 and TNF-α. Furthermore, sputum neutrophilia correlated with disease severity assessed by GOLD stages. Likewise the extent of TNF-α release from blood cells also positively correlated with the disease severity but negatively with that of sputum cell culture. Blood release of TNF-α and IL-6 negatively correlated with body mass index. Altogether, our results showed a significant relationship between cellular marker in blood and sputum but poor relationship between local and systemic release of cytokines. Conclusions: COPD is characterized by prominent neutrophilic inflammation and raised IFN-γ production at both bronchial and systemic level. Overproduction of TNF-α at systemic level correlates with disease severity and inversely with body mass index.

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Section: Discussionsupporting

confidence: 85%

Local and systemic cellular inflammation and cytokine release in chronic obstructive pulmonary disease

Moermans¹,

Heinen

Nguyen

et al. 2011

Cytokine

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“…TNF-a levels are increased in sputum of COPD patients [37], and weight loss in COPD has been associated with increased levels of circulating TNF-a [38]. The potential implications of the two TNF-a and Lt-a polymorphisms investigated have already been extensively discussed [1][2][3][5][6][7][8][9].…”

Section: Discussionmentioning

confidence: 99%

Tumour necrosis factor family genes in a phenotype of COPD associated with emphysema

Ferrarotti¹,

Zorzetto²,

Beccaria³

et al. 2003

Eur Respir J

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Genetic factors are believed to play a role in the individual susceptibility to chronic obstructive pulmonary disease (COPD). Tumour necrosis factor (TNF) family genes have been widely investigated but inconsistent results may lie either in the genetic heterogeneity of populations or in the poor phenotype definition. A genetic study was performed using a narrower phenotype of COPD.The authors studied 86 healthy smokers and 63 COPD subjects who were enrolled based on irreversible airflow obstruction (forced expiratory volume in one second/forced vital capacity v70% predicted) and a diffusing capacity for carbon monoxide v50% predicted (moderate-to-severe COPD associated with pulmonary emphysema). The following polymorphisms were investigated: TNF-308, the biallelic polymorphism located in the first intron of the lymphotoxin-a gene, and exon 1 and exon 6 of the TNF receptor 1 and 2 genes, respectively.No significant deviations were found concerning the four polymorphisms studied between the two populations.The authors confirm that the tumour necrosis factor family genes, at least for the polymorphisms investigated, are not major genetic risk factors for chronic obstructive pulmonary disease in Caucasians, either defined in terms of emphysema (this study) or airflow obstruction (previous studies). Nevertheless, the authors would like to emphasise the importance of narrowing the phenotype in the search for genetic risk factors in chronic obstructive pulmonary disease. Eur Respir J 2003; 21: 444-449.

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“…Tumour necrosis factor-a Plasma tumour necrosis factor (TNF)-a and its soluble receptor are increased in COPD patients [13][14][15], and TNF-a is also released from circulating cells in COPD patients with cachexia [16]. Circulating TNF-a appears to be related, at least in part, to hypoxaemia [14].…”

Section: Interleukin-6mentioning

confidence: 99%

Systemic manifestations and comorbidities of COPD

Barnes¹,

Celli²

2009

European Respiratory Journal

1,461

1,113

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Increasing evidence indicates that chronic obstructive pulmonary disease (COPD) is a complex disease involving more than airflow obstruction. Airflow obstruction has profound effects on cardiac function and gas exchange with systemic consequences. In addition, as COPD results from inflammation and/or alterations in repair mechanisms, the ''spill-over'' of inflammatory mediators into the circulation may result in important systemic manifestations of the disease, such as skeletal muscle wasting and cachexia. Systemic inflammation may also initiate or worsen comorbid diseases, such as ischaemic heart disease, heart failure, osteoporosis, normocytic anaemia, lung cancer, depression and diabetes. Comorbid diseases potentiate the morbidity of COPD, leading to increased hospitalisations, mortality and healthcare costs. Comorbidities complicate the management of COPD and need to be evaluated carefully. Current therapies for comorbid diseases, such as statins and peroxisome proliferator-activated receptor-agonists, may provide unexpected benefits for COPD patients. Treatment of COPD inflammation may concomitantly treat systemic inflammation and associated comorbidities. However, new broad-spectrum anti-inflammatory treatments, such as phosphodiesterase 4 inhibitors, have significant side-effects so it may be necessary to develop inhaled drugs in the future. Another approach is the reversal of corticosteroid resistance, for example with effective antioxidants. More research is needed on COPD comorbidities and their treatment.

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Tumor necrosis factor-alpha levels and weight loss in chronic obstructive pulmonary disease.

Cited by 434 publications

References 0 publications

Local and systemic cellular inflammation and cytokine release in chronic obstructive pulmonary disease

Local and systemic cellular inflammation and cytokine release in chronic obstructive pulmonary disease

Tumour necrosis factor family genes in a phenotype of COPD associated with emphysema

Systemic manifestations and comorbidities of COPD

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