Abstract
BackgroundChronic obstructive pulmonary disease (COPD) is associated with local and systemic inflammation. The knowledge of interaction and co-variation of the inflammatory responses in different compartments is meagre.MethodHealthy controls (n = 23), smokers with (n = 28) and without (n = 29) COPD performed spirometry and dental examinations. Saliva, induced sputum, bronchoalveolar lavage (BAL) fluid and serum were collected. Inflammatory markers were assessed in all compartments using ELISA, flow cytometry and RT-PCR.ResultsNegative correlations between lung function and saliva IL-8 and matrix metalloproteinase-9 (MMP-9) were found in smokers with COPD. IL-8 and MMP-9 in saliva correlated positively with periodontal disease as assessed by gingival bleeding in non-smokers.Tumor necrosis factor-α (TNF-α) in saliva, serum and TNF-α mRNA expression on macrophages in BAL-fluid were lower in smokers than in non-smokers. There were positive correlations between soluble TNF-α receptor 1 (sTNFR1) and soluble TNF-α receptor 2 (sTNFR2) in sputum, BAL-fluid and serum in all groups. Sputum interleukin-8 (IL-8) or interleukin-6 (IL-6) was positively correlated with sTNFR1 or sTNFR2 in non-smokers and with sTNFR2 in COPD.ConclusionSaliva which is convenient to collect and analyse, may be suitable for biomarker assessment of disease activity in COPD. An attenuated TNF-α expression was demonstrated by both protein and mRNA analyses in different compartments suggesting that TNF-α response is altered in moderate and severe COPD. Shedding of TNFR1 or TNFR2 is similarly regulated irrespective of airflow limitation.
Highlights
Chronic obstructive pulmonary disease (COPD) is characterized by airway inflammation, chronic airflow limitation, progressive tissue destruction, extra-pulmonary manifestations and systemic inflammation
IL-8 and matrix metalloproteinase-9 (MMP-9) in saliva correlated positively with periodontal disease as assessed by gingival bleeding in non-smokers
An attenuated tumor necrosis factor-α (TNF-α) expression was demonstrated by both protein and mRNA analyses in different compartments suggesting that TNF-α response is altered in moderate and severe COPD
Summary
Chronic obstructive pulmonary disease (COPD) is characterized by airway inflammation, chronic airflow limitation, progressive tissue destruction, extra-pulmonary manifestations and systemic inflammation. Several studies had shown the relationship between inflammatory biomarkers and exacerbations as well as systemic inflammation in COPD [1,2]. The inflammatory response in COPD is dominated by neutrophils and chemokines/cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-8 (IL-8), which are of importance for neutrophils recruitment [3]. Interleukin-6 (IL-6), a proinflammatory cytokine, is increased locally in the airways of the periodontal tissues. Smoking, which is the main risk factor for COPD, increases the risk for periodontal disease by 5 to 20 times [9]. There are epidemiological studies suggesting a co-variation between periodontal disease and COPD [10] but a causal relationship between the two diseases has not been convincingly demonstrated. Chronic obstructive pulmonary disease (COPD) is associated with local and systemic inflammation. The knowledge of interaction and co-variation of the inflammatory responses in different compartments is meagre
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