A panel of multiple markers associated with chronic systemic inflammation and the risk of atherogenesis is detectable in asthma and chronic obstructive pulmonary disease

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are both lung diseases involving chronic inflammation of the airway. The injury is reversible in asthma whereas it is mostly irreversible in COPD. Both patients of asthma and COPD are known at risk for cardiovascular disease (CVD) and type 2 diabetes (T2DM), nephropathy, and cancer. We measured multiple risk markers for atherogenesis in 55 patients with asthma and 62 patients with COPD. We wanted to know whether risk markers for atherogenesis corresponding to sequence of events of chronic inflammation were also detectable in the airway inflammatory diseases. Elevation of almost all markers involving inflammation of the endothelial cells in the coronary artery were detectable in asthma and COPD involving the inflammation of the epithelial cell lining of the airway. Both the level and % elevation of all markers were found mostly higher in COPD, the more severe form of the lung disease. We believe that these markers are useful for predicting risk of developing clinical complications such as CVD.

Systemic Inflammation in Older Adults With Asthma-COPD Overlap Syndrome

“…In the majority of previous reports of systemic inflammation in chronic airway disease, patients with asthma-COPD overlap syndrome were either not properly defined,19,20,21 or were specifically excluded, this may result in mixed study population of patients with (A) fixed airflow obstruction and, (B) both airflow reversibility and fixed obstruction, which may represent different disease pathogenesis. Furthermore, smoking history was used as an exclusion criterion and as a result a great number of patients were excluded from the studies 19,20,21,22. It is well known that studies, in particular randomised controlled trials (RCTs), in asthma and COPD are based on highly selected subgroups of people, however this does not reflect the spectrum of patient seen in practice23,24 leading to evidence gaps.…”

Signal Relay by CC Chemokine Receptor 2 (CCR2) and Formylpeptide Receptor 2 (Fpr2) in the Recruitment of Monocyte-derived Dendritic Cells in Allergic Airway Inflammation

“…This dynamic regulation of chemoattractant receptors on myeloid cells including DCs represents an important host response during disease states (38). In the inflamed lung, recruited inflammatory DCs immediately encounter a variety of bacteria-and host-derived TLR agonists such as LPS, PGN, HMGB1, fragment of fibronectin, and hyaluronic acid oligosaccharides (31,39,40), which reduce CCR2 but increase Fpr2 expression and function, enabling the cells to reach small airways in response to the Fpr2 agonist CRAMP produced in the inflamed tissue (41)(42)(43)(44).…”

Pulmonary Remodeling in Equine Asthma: What Do We Know about Mediators of Inflammation in the Horse?

“…Human asthma is considered to be a systemic disease, as an increase in several inflammatory markers has been observed in the blood of affected patients [16]. These include immunity-related mediators (cytokines, eicosanoids, cyclooxygenase products, and IgEs) and the acute phase markers C-reactive protein, haptoglobin, fibrinogen, and serum amyloid A [78–80]. Systemic inflammation in patients with chronic airway diseases is thought to contribute to comorbidities [16, 81–84].…”