Inflammatory parameters and pulmonary biomarkers in smokers with and without chronic obstructive pulmonary disease (COPD)

Abstract

Background: We organized this study in order to investigate differences in serum inflammatory profiles and circulating serum pneumoproteins between smokers with and without chronic obstructive pulmonary disease (COPD). Methods: Patients aged 35-70 years with COPD and a smoking history ≥10 pack-years (cases, n=38) and 38 participants with the same smoking history without COPD (controls) were included in a comparative study conducted as part of a population-based cross-sectional study with 2,388 individuals in northwestern Russia. Cases and controls were matched for age and smoking history. Airflow obstruction (AO) was defined using forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) <0.70 and/or FEV1/FVC < lower limit of the normal cut-off values. Patients at risk for COPD were reassessed using a standardized diagnostic work-up protocol. Several parameters, among which four inflammatory biomarkers [the highsensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, IL-8, and tumor necrosis factor-α (TNF-α) levels] and two pneumoproteins [surfactant protein D (SP-D) and Clara cell secretory protein 16 (CC16)], were measured in the peripheral blood. Systemic inflammation was defined as at least 2 or more elevated biomarker levels. Results: Out of all smokers, 57.9% with normal spirometry and 36.8% with COPD did not have systemic inflammation, whereas 44.7% of the patients with COPD and 5.3% of the patients without AO demonstrated at least two elevated biomarker levels. No difference in age, gender, and smoking history, environmental and occupational exposure was found between the non-inflamed and the inflamed smokers.Of all risk factors studied, only COPD was associated with systemic inflammation [odds ratio (OR) 11.42, 95% confidence interval (CI): 2.13-58.84].Conclusions: Our study describes the systemic inflammatory network pattern associated with COPD and how it differs from the pattern in smokers with normal lung function. Systemic inflammation is not present in all smokers with COPD; in contrast, some non-obstructed smokers are characterized by systemic inflammation. From this perspective, smoking itself could be seen as a disease and studied accordingly.Trial registration: NCT02307799.

Multiple Chronic Diseases Associated With Tooth Loss Among the US Adult Population

“…Asthma may contribute less significantly to systemic inflammation due to the short onset of episodes of acute asthma attacks. Previous studies indicated that COPD significantly increases the systemic inflammatory burden, which could be further amplified by smoking (Qian et al, 2020;Andreeva et al, 2021). Smoking is a well-known risk factor for COPD and heart disease, as well as tooth loss (Cunningham et al, 2016).…”

Impact of JAK/STAT inhibitors on human monocyte‐derived‐macrophages stimulated by cigarette smoke extract and lipopolysaccharide

“…Macrophages, particularly alveolar macrophages, are the most abundant type of immune cell seem to accumulate in areas of tissue damage in the lungs 3 . This increase in the number of macrophages may be due to active recruitment of circulating monocytes as a result of the chemoattractant actions of CCL2 and CXCL1 22,23 . CXCL8 concentrations are also increased in induced sputum of patients with COPD and increase further during exacerbations 22,24,25 .…”

“…This increase in the number of macrophages may be due to active recruitment of circulating monocytes as a result of the chemoattractant actions of CCL2 and CXCL1 22,23 . CXCL8 concentrations are also increased in induced sputum of patients with COPD and increase further during exacerbations 22,24,25 . CXCL8 is secreted from macrophages, T cells, epithelial cells, and neutrophils and is chemotactic for neutrophils 26,27 …”

“…22,23 CXCL8 concentrations are also increased in induced sputum of patients with COPD and increase further during exacerbations. 22,24,25 CXCL8 is secreted from macrophages, T cells, epithelial cells, and neutrophils and is chemotactic for neutrophils. 26,27 Serpin E1, also known as plasminogen activator inhibitor-1 (PAI-1) was also strongly increased.…”

Effect of statins on pulmonary function in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis of randomized controlled trials

“…Therefore, statins inhibit thrombotic responses ( 4 - 6 ). Statins have anti-inflammatory and immunomodulatory effects, which can reduce the levels of inflammatory markers [such as C-reactive protein (CRP)] in the serum, improve vascular endothelial function, reduce the infiltration and adhesion of inflammatory cells, and inhibit the production of inflammatory factors such as tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) ( 7 , 8 ). Studies have shown that statins attenuate the progression of PH in several animal models ( 9 - 11 ).…”