scholarly journals Association of TNF-α–308G/A, SP-B 1580 C/T, IL-13 –1055 C/T gene polymorphisms and latent adenoviral infection with chronic obstructive pulmonary disease in an Egyptian population

2012 ◽  
Vol 2 ◽  
pp. 286-295 ◽  
Author(s):  
Nada Ezzeldin ◽  
Alaa Shalaby ◽  
Amal Saad-Hussein ◽  
Howayda Ezzeldin ◽  
Dalia El Lebedy ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Adenoviral Infection ◽  
Egyptian Population ◽  
Tnf Α

The role of gene polymorphisms in the pathogenesis of chronic obstructive pulmonary disease

Biologia ◽  
2008 ◽  
Vol 63 (1) ◽  
Author(s):  
Eva Slabá ◽  
Pavol Joppa ◽  
Ján Šalagovič ◽  
Ružena Tkáčová
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Inflammatory Response ◽  
Candidate Genes ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Association Studies ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Positional Candidate ◽  
Linkage Analyses

AbstractChronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Irreversible airflow limitation, both progressive and associated with an inflammatory response of the lungs to noxious particles or gases, is a hallmark of the disease. Cigarette smoking is the most important environmental risk factor for COPD, nevertheless, only approximately 20–30% of smokers develop symptomatic disease. Epidemiological studies, case-control studies in relatives of patients with COPD, and twin studies suggest that COPD is a genetically complex disease with environmental factors and many involved genes interacting together. Two major strategies have been employed to identify the genes and the polymorphisms that likely contribute to the development of complex diseases: association studies and linkage analyses. Biologically plausible pathogenetic mechanisms are prerequisites to focus the search for genes of known function in association studies. Protease-antiprotease imbalance, generation of oxidative stress, and chronic inflammation are recognized as the principal mechanisms leading to irreversible airflow obstruction and parenchymal destruction in the lung. Therefore, genes which have been implicated in the pathogenesis of COPD are involved in antiproteolysis, antioxidant barrier and metabolism of xenobiotic substances, inflammatory response to cigarette smoke, airway hyperresponsiveness, and pulmonary vascular remodelling. Significant associations with COPD-related phenotypes have been reported for polymorphisms in genes coding for matrix metalloproteinases, microsomal epoxide hydrolase, glutathione-S-transferases, heme oxygenase, tumor necrosis factor, interleukines 1, 8, and 13, vitamin D-binding protein and β-2-adrenergic receptor (ADRB2), whereas adequately powered replication studies failed to confirm most of the previously observed associations. Genome-wide linkage analyses provide us with a novel tool to identify the general locations of COPD susceptibility genes, and should be followed by association analyses of positional candidate genes from COPD pathophysiology, positional candidate genes selected from gene expression studies, or dense single nucleotide polymorphism panels across regions of linkage. Haplotype analyses of genes with multiple polymorphic sites in linkage disequilibrium, such as the ADRB2 gene, provide another promising field that has yet to be explored in patients with COPD. In the present article we review the current knowledge about gene polymorphisms that have been recently linked to the risk of developing COPD and/or may account for variations in the disease course.

scholarly journals Metabolic Phenotype and Adipose Tissue Inflammation in Patients with Chronic Obstructive Pulmonary Disease

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Peter Skyba ◽  
Jozef Ukropec ◽  
Pavol Pobeha ◽  
Barbara Ukropcova ◽  
Pavol Joppa ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Pulmonary Disease ◽  
Normal Weight ◽  
Cell Surface Receptor ◽  
Metabolic Phenotype ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α

Potential links between metabolic derangements and adipose tissue (AT) inflammation in patients with chronic obstructive pulmonary disease (COPD) are unexplored. We investigated AT expressions of interleukin (IL)-6, tumor necrosis factor (TNF)-α, CD68 (macrophage cell surface receptor), caspase-3, and Bax, and their relationships to the metabolic phenotype in nine cachectic, 12 normal-weight, 12 overweight, and 11 obese patients with COPD (age62.3±7.2years). With increasing body mass index, increases in AT expressions of IL-6, TNF-α, and CD68 were observed (P<.001;P=.005;P<.001, resp.), in association with reduced insulin sensitivity (P<.001). No differences were observed between cachectic and normal-weight patients in AT expressions of inflammatory or proapoptotic markers. Adipose tissue CD68 and TNF-α expressions predicted insulin sensitivity independently of known confounders (P=.005;P=.025;R2=0.840). Our results suggest that AT inflammation in obese COPD patients relates to insulin resistance. Cachectic patients remain insulin sensitive, with no AT upregulation of inflammatory or proapoptotic markers.

CTLA4 and CD86 gene polymorphisms and susceptibility to chronic obstructive pulmonary disease

2010 ◽  
Vol 71 (11) ◽  
pp. 1141-1146 ◽  
Author(s):  
Yun Liu ◽  
Wei-Bo Liang ◽  
Lin-Bo Gao ◽  
Xin-Min Pan ◽  
Tian-Yi Chen ◽  
...  
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Gene Polymorphisms ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease

scholarly journals The influence of various regimens of treatment on the level of proinflammatory cytokine TNF-alpha in induced sputum in case of an exacerbation of chronic obstructive pulmonary disease (copd) in persons, who suffered from pulmonary tuberculosis

2013 ◽  
Vol 17 (1 (65)) ◽  
pp. 38-40
Author(s):  
Ya. V. Ivanova
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Tuberculosis ◽  
Pulmonary Disease ◽  
Proinflammatory Cytokine ◽  
Combined Treatment ◽  
Induced Sputum ◽  
Tnf Alpha ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Tnf Α

The influence of various regimens of treatment of the regional (in induced sputum) level of proinflammatory cytokine TNF-α in patients with chronic obstructive pulmonary disease (COPD), who have suffered from pulmonary tuberculosis (PT), has been studied. An advantage of using a combined treatment of COPD exacerbation by means of β2agonist and an anticholinergic preparation (berodual), and also doxofillin (aerofillin) for the purpose of correcting regional (endobronchial) imbalance of cytokine homeostasis is proved.

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