scholarly journals Mendelian Randomization Study of Interleukin-6 in Chronic Obstructive Pulmonary Disease

Respiration ◽  
2011 ◽  
Vol 82 (6) ◽  
pp. 530-538 ◽  
Author(s):  
Yannick M.T.A. van Durme ◽  
Lies Lahousse ◽  
Katia M.C. Verhamme ◽  
Lisette Stolk ◽  
Mark Eijgelsheim ◽  
...  
2013 ◽  
Vol 14 (1) ◽  
pp. 24 ◽  
Author(s):  
Renata Ferrari ◽  
Suzana E Tanni ◽  
Laura MO Caram ◽  
Corina Corrêa ◽  
Camila R Corrêa ◽  
...  

Author(s):  
Татьяна Виткина ◽  
Tatyana Vitkina ◽  
К Сидлецкая ◽  
K Sidleckaya

The review focuses on the role of interleukin-6 (IL-6) signaling in the development of a systemic inflammatory process in chronic obstructive pulmonary disease (COPD). In most researches the attention is paid to local inflammation in COPD. However, it is known that the pathology is characterized by a systemic inflammatory process, which is manifested in the increased levels of proinflammatory mediators in blood flow, and the study of the molecular mechanisms of its development is very important for the therapy of the disease. One of the key mediators of systemic inflammation is cytokine IL-6 which has pro- and antiinflammatory properties. Its effect on the cells is determined by the type of signaling. Nowadays three types of IL-6 signaling are identified: transsignaling, classical and cluster signaling. The review presents the known pathophysiological mechanisms of the development of systemic inflammation in COPD involving IL-6. As a proinflammatory cytokine, IL-6 performs the following functions: transmission of a signal on lung tissue damage, initiation of leukocyte migration into the inflammation site, inhibition of T-cell apoptosis into the inflammation site, influence on T helper differentiation, participation in pathophysiological reactions of development of emphysema and fibrosis. The significance of IL-6 transsignaling for the development of inflammation in COPD has been confirmed by many studies, while there are practically no works devoted to the study of classical IL-6 signaling in COPD. The data presented in the review indicate the need for further study of the role of different types of IL-6 signaling, especially classical signaling, in the regulation of systemic inflammation in COPD.


2020 ◽  
Vol 17 (7) ◽  
pp. 3097-3103
Author(s):  
Theopilus Obed Lay ◽  
Muhammad Amin

Chronic obstructive pulmonary disease (COPD) is known as a chronic inflammatory disease that not only occurs in the lung, but also affects the systemic. A continuous chronic inflammation in COPD patients will have an increased proinflammatory cytokines, both in COPD patients’ respiratory tract and blood. Interleukin-6 (IL-6) is one of proinflammatory cytokines that increases with COPD progression. IL-6 level examination in COPD patient’s blood as a systemic inflammation indicator is convenient and quick. The research aimed to measure IL-6 level in COPD patient’s serum, to determine COPD severity level, and to analyze correlation between IL-6 and severity level. The research is an observational analytic study using cross sectional design. The samples were 38 non-exacerbated COPD outpatients who visited Lung Unit at Dr. Soetomo Teaching Hospital, Surabaya, Indonesia and met inclusion and exclusion criteria. The study found no significant correlation between IL-6, COPD severity level, COPD obstruction, first forced expiratory volume (FEV1), and FEV1/forced vital capacity (FVC), with p > 0.05. There was a significant correlation between IL-6 level, body mass index (BMI), and COPD assessment test (CAT) score, with p < 0.05, while there was no significant difference of IL-6 level between high-risk and low-risk patients, with p = 0.066 (p > 0.05). Moreover, there was a significant difference of IL-6 level between group A and D, with p = 0.040 (p < 0.05). There were no significant correlation and difference between COPD severities, COPD obstruction, FEV1, FVC, FEV1/FEC ratio, smoking duration with stable IL-6.


2019 ◽  
Author(s):  
Jenny C Censin ◽  
Jonas Bovijn ◽  
Teresa Ferreira ◽  
Sara L Pulit ◽  
Reedik Mägi ◽  
...  

AbstractBackgroundObesity traits are causally implicated with risk of cardiometabolic diseases. It remains unclear whether there are similar causal effects of obesity traits on other non-communicable diseases. Also, it is largely unexplored whether there are any sex-specific differences in the causal effects of obesity traits on cardiometabolic diseases and other leading causes of death. We therefore tested associations of sex-specific genetic risk scores (GRSs) for body mass index (BMI), waist-hip-ratio (WHR), and WHR adjusted for BMI (WHRadjBMI) with leading causes of mortality, using a Mendelian randomization (MR) framework.Methods and FindingsWe constructed sex-specific GRSs for BMI, WHR, and WHRadjBMI, including 565, 324, and 338 genetic variants, respectively. These GRSs were then used as instrumental variables to assess associations between the obesity traits and leading causes of mortality using an MR design in up to 422,414 participants from the UK Biobank. We also investigated associations with potential mediators and risk factors, including smoking, glycemic and blood pressure traits. Sex-differences were subsequently assessed by Cochran’s Q-test (Phet).Up to 227,717 women and 194,697 men with mean (standard deviation) age 56.6 (7.9) and 57.0 (8.1) years, body mass index 27.0 (5.1) and 27.9 (4.2) kg/m2and waist-hip-ratio 0.82 (0.07) and 0.94 (0.07), respectively, were included. Mendelian randomization analysis showed that obesity causes coronary artery disease, stroke (particularly ischemic), chronic obstructive pulmonary disease, lung cancer, type 2 and 1 diabetes mellitus, non-alcoholic fatty liver disease, chronic liver disease, and acute and chronic renal failure. A 1 standard deviation higher body mass index led to higher risk of type 2 diabetes in women (OR 3.81; 95% CI 3.42-4.25, P=8.9×10−130) than in men (OR 2.78; 95% CI 2.57-3.02, P=1.0×10−133, Phet=5.1×10−6). Waist-hip-ratio led to a higher risk of chronic obstructive pulmonary disease (Phet=5.5×10−6) and higher risk of chronic renal failure (Phet=1.3×10−4) in men than women.A limitation of MR studies is potential bias if the genetic variants are directly associated with confounders (pleiotropy), but sensitivity analyses such as MR-Egger supported the main findings. Our study was also limited to people of European descent and results may differ in people of other ancestries.ConclusionsObesity traits have an etiological role in the majority of the leading global causes of death. Sex differences exist in the effects of obesity traits on risk of type 2 diabetes, chronic obstructive pulmonary disease, and renal failure, which may have implications on public health.


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