Airway inflammatory markers in chronic obstructive pulmonary disease patients and healthy smokers

Background: Cigarette smoke with its toxic ingredients leads to chronic inflammations in the airways.Objectives: In this study, the effect of cigarette smoke on the levels of inflammatory markers, interleukin.6 (IL.6), interleukin.8 (IL.8), and tumor necrosis factor.alpha (TNF.ƒ¿) in induced sputum was investigated.Materials and Methods: Twenty patients with chronic obstructive pulmonary disease (COPD) (group I), 20 healthy smokers (group II), and 20 healthy nonsmokers (group III) were included in the study. The levels of IL.6, IL.8, and TNF.ƒ¿ in induced sputum were measured in these groups, and comparison analysis between the groups and correlation analysis for smoking load (pack.years) and spirometric parameters were performed.Results: Mean age of the patients in groups I, II, and III were 61.2 } 1.7, 58.2 } 1.6, and 59.1 } 5.4 years, respectively (P > 0.05). Smoking loads of group I and group II were 38.6 } 2.1 and 29.5 } 2.3 pack.years, respectively (P < 0.05). All cytokine levels were significantly higher in group I than groups II and III (P < 0.05). In addition to this, mean cytokineslevels were significantly higher in group II than group III (P < 0.05). Smoking load of group II subjects was positively correlated with IL.6, IL.8, and TNF.ƒ¿ in induced sputum (P < 0.05).Conclusions: We found that inflammatory marker levels in induced sputum were significantly higher in COPD patients and smokers than nonsmokers. Moreover, there was a moderate positive correlation between IL.6, IL.8, and TNF.ƒ¿ levels and smoking load in the healthy smokers. We think that further studies are needed to determine whether higher levels of cytokine levels in sputum might be helpful in predicting the healthy smokers who will develop COPD in future.Key words: Chronic obstructive pulmonary disease, inflammatory markers, induced sputum, IL.6, IL.8, TNF.ƒ

Elevation of IL-6 in the allergic asthmatic airway is independent of inflammation but associates with loss of central airway function

<p>Abstract</p> <p>Background</p> <p>Asthma is a chronic inflammatory disease of the airway that is characterized by a Th2-type of immune response with increasing evidence for involvement of Th17 cells. The role of IL-6 in promoting effector T cell subsets suggest that IL-6 may play a functional role in asthma. Classically IL-6 has been viewed as an inflammatory marker, along with TNFα and IL-1β, rather than as regulatory cytokine.</p> <p>Objective</p> <p>To investigate the potential relationship between IL-6 and other proinflammatory cytokines, Th2/Th17 cytokines and lung function in allergic asthma, and thus evaluate the potential role of IL-6 in this disease.</p> <p>Methods</p> <p>Cytokine levels in induced sputum and lung function were measured in 16 healthy control and 18 mild-moderate allergic asthmatic subjects.</p> <p>Results</p> <p>The levels of the proinflammatory biomarkers TNFα and IL-1β were not different between the control and asthmatic group. In contrast, IL-6 levels were specifically elevated in asthmatic subjects compared with healthy controls (p < 0.01). Hierarchical regression analysis in the total study cohort indicates that the relationship between asthma and lung function could be mediated by IL-6. Among Th2 cytokines only IL-13 (p < 0.05) was also elevated in the asthmatic group, and positively correlated with IL-6 levels (r_S= 0.53, p < 0.05).</p> <p>Conclusions</p> <p>In mild-moderate asthma, IL-6 dissociates from other proinflammatory biomarkers, but correlates with IL-13 levels. Furthermore, IL-6 may contribute to impaired lung function in allergic asthma.</p

Targeting IL-1β and IL-17A driven inflammation during influenza-induced exacerbations of chronic lung inflammation.

For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation