Approximately 15,000 liters of air transit through the respiratory tract during respiration on a daily basis. The epithelium of the pulmonary airways plays a prominent role in protecting us against detrimental agents since it is continually exposed to particles that are potentially harmful for the lungs including microorganisms, dust and air pollutants. However, via mucociliary clearance and coughing, these agents are eliminated and airway integrity is protected from these potentially damaging attacks.
Until recently, the epithelium of the respiratory tract was only seen as a physical barrier, macrophages being considered as the main immune sensor of inflammation and damage in the respiratory tract. Although its structural integrity is essential, it is now well established that the airway epithelium plays a major role in triggering an innate immune response to protect the lung from infection and injury in various chronic respiratory diseases. Airway epithelial cells express receptors to detect microorganisms, including Toll-Like Receptors (TLRs) and Nucleotide-binding oligomerization domain-like receptors (NLRs) to trigger an innate immune response. In addition, they secrete defense molecules, for instance mucins, anti-microbial peptides and surfactant proteins that act to maintain homeostasis in the lung. Interestingly, defects in these mechanisms are associated with chronic lung pathologies such as cystic fibrosis, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and asthma.
Previously considered as almost sterile, the recent discovery of a lung microbiome via new sequencing technologies has changed our conception of how the development of a lung disease may occur or evolve according to changes (imbalance/dysbiosis) in the microbiota. Besides descriptive and correlative studies about these changes, it is still unknown at the molecular level how the microbiota, either physiologic or pathogenic, interact with the lung mucosa and how this impacts on mucosal immunity in the lung.
In this Research Topic, we aim to assemble a series of articles that highlight how the airway epithelium is essential in the onset and modulation of the innate immune system in chronic lung diseases including, but not limited to, cystic fibrosis, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and asthma. We will also explore the interplay between the lung microbiome and the airway epithelium
We welcome the submission of Reviews, Mini-Reviews and Original Research articles that cover, but are not limited to, the following topics:
1. The biological functions of the airway epithelial barrier in regulating immunity.
2. Abnormal crosstalk between the commensal microbiota and the immune system in the lung.
3. Therapeutic interventions aimed at restoring airway barrier integrity and lung immune homeostasis such as anti-inflammatory molecules.
Approximately 15,000 liters of air transit through the respiratory tract during respiration on a daily basis. The epithelium of the pulmonary airways plays a prominent role in protecting us against detrimental agents since it is continually exposed to particles that are potentially harmful for the lungs including microorganisms, dust and air pollutants. However, via mucociliary clearance and coughing, these agents are eliminated and airway integrity is protected from these potentially damaging attacks.
Until recently, the epithelium of the respiratory tract was only seen as a physical barrier, macrophages being considered as the main immune sensor of inflammation and damage in the respiratory tract. Although its structural integrity is essential, it is now well established that the airway epithelium plays a major role in triggering an innate immune response to protect the lung from infection and injury in various chronic respiratory diseases. Airway epithelial cells express receptors to detect microorganisms, including Toll-Like Receptors (TLRs) and Nucleotide-binding oligomerization domain-like receptors (NLRs) to trigger an innate immune response. In addition, they secrete defense molecules, for instance mucins, anti-microbial peptides and surfactant proteins that act to maintain homeostasis in the lung. Interestingly, defects in these mechanisms are associated with chronic lung pathologies such as cystic fibrosis, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and asthma.
Previously considered as almost sterile, the recent discovery of a lung microbiome via new sequencing technologies has changed our conception of how the development of a lung disease may occur or evolve according to changes (imbalance/dysbiosis) in the microbiota. Besides descriptive and correlative studies about these changes, it is still unknown at the molecular level how the microbiota, either physiologic or pathogenic, interact with the lung mucosa and how this impacts on mucosal immunity in the lung.
In this Research Topic, we aim to assemble a series of articles that highlight how the airway epithelium is essential in the onset and modulation of the innate immune system in chronic lung diseases including, but not limited to, cystic fibrosis, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis and asthma. We will also explore the interplay between the lung microbiome and the airway epithelium
We welcome the submission of Reviews, Mini-Reviews and Original Research articles that cover, but are not limited to, the following topics:
1. The biological functions of the airway epithelial barrier in regulating immunity.
2. Abnormal crosstalk between the commensal microbiota and the immune system in the lung.
3. Therapeutic interventions aimed at restoring airway barrier integrity and lung immune homeostasis such as anti-inflammatory molecules.
