The airway epithelium serves as both a physical barrier and as an active contributor in maintaining immune defense. Upon exposure to external insults such as injury and infection, the epithelium releases alarmins including interleukin-25 (IL-25), IL-33, and thymic stromal lymphopoietin (TSLP), which assist in initiating and amplifying the immune response. Complementing these are the collectins, particularly surfactant protein-D (SP-D), which also participate in the innate immune response. SP-D along with its closely related collectin, SP-A, bind pathogens, apoptotic cells, and allergens, promoting phagocytosis while modulating inflammation and preventing excessive Th2-driven responses. This review discusses the role of the airway epithelium in host defense mechanisms, particularly in chronic obstructive pulmonary disease (COPD) and asthma, and explores the therapeutic implications of epithelial-driven immune responses in respiratory inflammation.
1 Introduction
The airway epithelium plays a crucial role in maintaining lung homeostasis, serving as both a physical barrier and an active participant in immune defense. In response to external stimuli, it releases epithelial-derived alarmins that initiate a cascade of immune responses, a topic that has received intensive consideration in recent years. This present review discusses the role of the airway epithelium in host defense mechanisms, particularly in COPD and asthma, and explores the therapeutic implications of epithelial-driven immune responses in respiratory inflammation. In particular, we address the roles of collectins and their complementary roles to those of alarmins. Although many factors contribute to both homeostasis and the development and chronicity of airway diseases, including members of the interferon (IFN) family, we focus on the roles of collectins and how they interplay with those key alarmins.
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