Abstract
Cytokines are key players in the initiation and propagation of inflammation in chronic inflammatory airway diseases such as chronic obstructive pulmonary disease (COPD), bronchiectasis and allergic asthma. This makes them attractive targets for specific novel anti-inflammatory treatment strategies. Recently, both interleukin-1 (IL-1) and IL-6 have been associated with negative health outcomes, mortality and a pro-inflammatory phenotype in COPD. IL-6 in COPD was shown to correlate negatively with lung function, and IL-1beta was induced by cigarette smoke in the bronchial epithelium, causing airway inflammation. Furthermore, IL-8 has been shown to be a pro-inflammatory marker in bronchiectasis, COPD and allergic asthma. Clinical trials using specific cytokine blockade therapies are currently emerging and have contributed to reduce exacerbations and steroid use in COPD. Here, we present a review of the current understanding of the roles of cytokines in the pathophysiology of chronic inflammatory airway diseases. Furthermore, outcomes of clinical trials in cytokine blockade as novel treatment strategies for selected patient populations with those diseases will be discussed.
Highlights
Chronic respiratory diseases account for 4.7% of global disability-adjusted life years with asthma and chronic obstructive pulmonary disease (COPD) being the most frequent, and chronic airway inflammation being one of the key processes involved in their pathogenesis [1,2]
The highest serum levels were found in patients with COPD stages III and IV according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) [46]
With chronic airway inflammation and remodeling serving as key factors for the severity of asthma, COPD, and bronchiectasis, three classes of inhaled therapies have been utilized to aid in symptom management
Summary
Chronic respiratory diseases account for 4.7% of global disability-adjusted life years with asthma and chronic obstructive pulmonary disease (COPD) being the most frequent, and chronic airway inflammation being one of the key processes involved in their pathogenesis [1,2]. Macrophages are located in airways, alveoli and the lung interstitium, and have the ability to migrate to the lung microvasculature, thereby modulating acute and chronic inflammatory responses [3] They are a main source of cytokines and inflammatory mediators, in addition to phagocytosing bacteria and apoptotic cells, and promote neutrophil accumulation [4]. The bronchial mucosa consists of a muco-ciliated, pseudostratified epithelium with predominantly ciliated cells, as well as mucus-secreting goblet cells (5–15%) in the large airways and basal cells/club cells in the smaller airways [15,16,17] It represents a physical and chemical barrier by: (1) apical junctions lining the upper and lower airways, (2) mucociliary clearance, and (3) secretion of mediators regulating inflammation, chemotaxis, and antimicrobial defense as mentioned above [18,19,20,21,22]. In chronic inflammatory airway diseases, epithelial dysfunction is one of the key features leading to altered epithelial integrity and disrupted physical, chemical, and immune barrier functions [23]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
