Why are patients with chronic obstructive pulmonary disease at increased risk of cardiovascular diseases? The potential role of systemic inflammation in chronic obstructive pulmonary disease

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.

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Systemic Inflammation in Chronic Obstructive Pulmonary Disease: May Adipose Tissue Play a Role? Review of the Literature and Future Perspectives

Mediators of Inflammation ◽

10.1155/2010/585989 ◽

2010 ◽

Vol 2010 ◽

pp. 1-11 ◽

Cited By ~ 33

Author(s):

Ruzena Tkacova

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Adipose Tissue ◽

Pulmonary Disease ◽

Systemic Inflammation ◽

Chronic Obstructive ◽

Adipose Tissue Inflammation ◽

Obstructive Pulmonary Disease ◽

Systemic Hypoxia ◽

Inflammatory Syndrome

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality worldwide. Low-grade systemic inflammation is considered a hallmark of COPD that potentially links COPD to increased rate of systemic manifestations of the disease. Obesity with/without the metabolic syndrome and cachexia represent two poles of metabolic abnormalities that may relate to systemic inflammation. On one hand systemic inflammatory syndrome likely reflects inflammation in the lungs, i.e. results from lung-to plasma spillover of inflammatory mediators. On the other hand, obesity-related hypoxia results in local inflammatory response within adipose tissueper se, and may contribute to elevations in circulatory mediators by spillover from the adipose tissue to the systemic compartment. The extent to which systemic hypoxia contributes to the adipose tissue inflammation remains unknown. We assume that in patients with COPD and concurrent obesity at least three factors play a role in the systemic inflammatory syndrome: the severity of pulmonary impairment, the degree of obesity-related adipose tissue hypoxia, and the severity of systemic hypoxia due to reduced pulmonary functions. The present review summarizes the epidemiological and clinical evidence linking COPD to obesity, the role of adipose tissue as an endocrine organ, and the role of hypoxia in adipose tissue inflammation.

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Assessment of Some Inflammatory Biomarkers as Predictors of Outcome of Acute Respiratory Failure on Top of Chronic Obstructive Pulmonary Disease and Evaluation of the Role of Bacteria

ISRN Microbiology ◽

10.5402/2012/240841 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 1

Author(s):

Hanaa Ahmed Shafiek ◽

Nashwa Hassan Abd-Elwahab ◽

Manal Mohammad Baddour ◽

Mohamed Mabrouk El-Hoffy ◽

Akram Abd-Elmoneim Degady ◽

...

Keyword(s):

Chronic Obstructive Pulmonary Disease ◽

Respiratory Failure ◽

Acute Respiratory Failure ◽

Pulmonary Disease ◽

Systemic Inflammation ◽

Wide Spectrum ◽

Chronic Obstructive ◽

Obstructive Pulmonary Disease ◽

Gram Negative

Objective. To study the value of the inflammatory markers (interleukin-6 (IL-6), interleukin-8 (IL-8), and C-reactive protein (CRP)) in predicting the outcome of noninvasive ventilation (NIV) in the management of acute respiratory failure (ARF) on top of chronic obstructive pulmonary disease (COPD) and the role of bacteria in the systemic inflammation. Methods. Thirty three patients were subjected to standard treatment plus NIV, and accordingly, they were classified into responders and nonresponders. Serum samples were collected for IL-6, IL-8, and CRP analysis. Sputum samples were taken for microbiological evaluation. Results. A wide spectrum of bacteria was revealed; Gram-negative and atypical bacteria were the most common (31% and 28% resp.; single or copathogen). IL-8 and dyspnea grade was significantly higher in the non-responder group ( and 0.023 resp.). IL-6 correlated positivity with the presence of infection and type of pathogen ( and 0.034 resp.). Gram-negative bacteria were associated with higher significant IL-6 in comparison between others ( pg/dL; ) but insignificantly affected NIV outcome (). Conclusions. High systemic inflammation could predict failure of NIV. G-ve bacteria correlated with high IL-6 but did not affect the response to NIV.

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