Early local immune defences in the respiratory tract

Abstract

Preface The respiratory immune response consists of multiple tiers of cellular responses that are engaged in a sequential manner in order to control infections. Stepwise engagement of effector functions with progressively increasing host fitness costs limits tissue damage. In addition, specific mechanisms are in place to promote disease tolerance in response to respiratory infections. Environmental factors, obesity and the ageing process can alter the efficiency and regulation of this tiered response, increasing pathology and mortality as a result. In this Review, we describe the cell types that coordinate pathogen clearance and tissue repair through serial secretion of cytokines, and discuss how the environment and comorbidity influence this response.

Loss of VAMP5 in mice results in duplication of the ureter and insufficient expansion of the lung

“…VAMP5 was abundant in the intrapulmonary airway epithelium (Fig. The club cells are secretory cells and a major epithelial cell type in the mouse intrapulmonary airway (Iwasaki et al, 2016). VAMP5 was localized in the basal cytoplasm of the epithelial cells (Fig.…”

Lung epithelium: barrier immunity to inhaled fungi and driver of fungal-associated allergic asthma

“…Several excellent reviews have been written on the topics of lung epithelial cell development and maintenance [9], pulmonary barrier immunity to bacterial and viral pathogens [10, 11], and epithelium-dependent allergic responses to model allergens, such as ovalbumin and house dust mite extracts [12]. This review will discuss recent advances in our understanding of how epithelial cells recognize and respond to the threat of fungal invasion and promote antifungal immunity.…”

Attenuation of interferon regulatory factor 7 activity in local infectious sites of trachea and lung for preventing the development of acute lung injury caused by influenza A virus

“…During the infection, IAV primarily targets the epithelial cells of the respiratory tract, and also infects local resident macrophages and dendritic cells . To respond, these infected cells all produce type I IFNs; resident macrophages are the predominant producers . The massively produced type I IFNs bind to the IFN‐ α and IFN‐ β receptor (IFNAR) on local epithelial cells and macrophages and initiate the Janus kinase—signal transducer and activator of transcription signalling pathway to activate IFN‐stimulated genes (ISGs), including genes for chemokines [e.g.…”

“…Among the members, IRF3 and IRF7 are major transcription factors of type I IFN genes . IRF3 is constitutively expressed in most cell types, whereas the basal IRF7 expression is limited to cell types such as macrophages and plasmacytoid dendritic cells . Upon IAV infection, the viral single‐stranded RNA can activate Toll‐like receptor 7 and its downstream signalling, leading to the activation of TANK binding kinase 1 (TBK1) or I κ B kinase ε (IKK ε ).…”