Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, no other organ has been as much in the focus of research as the lung. However, many other causes may also lead to inflammation and severe damage of the lung, potentially leading to life-threatening acute respiratory distress syndrome (ARDS). The loss of alveolar-capillary barrier integrity plays a pivotal role in the pathogenesis of respiratory inflammation and failure. Moreover, repair of the injured air-blood barrier is key for recovery. Endocytic and trafficking events in alveolar epithelial and endothelial cells, the major components of this barrier, as well as in neutrophils and macrophages, which predominantly regulate pulmonary inflammation, are centrally involved in both the emergence of and recovery from lung damage.
The primary goal of this Research Topic is to enhance our understanding regarding the role of endocytosis and trafficking in regulation of alveolar-capillary barrier integrity. Recent technological advances enable dissection of the precise lung cell-specific molecular patterns of these events in complex lung model systems. For example, recent evidence suggests that both entry and propagation of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), influenza virus and respiratory syncytial virus are mediated by spatiotemporally-specific epithelial endocytic processes. Furthermore, protein-rich pulmonary edema secondary to virus-induced lung damage is cleared from the alveolar space by well-defined endocytic processes that critically influence survival of patients with ARDS. Moreover, endothelial barrier integrity in the lung is maintained in part by adherens junction proteins, expression of which at the cell surface is tightly regulated by endocytic trafficking. Finally, uptake and intracellular processing of engineered nanoparticles during targeted delivery of drugs to the alveolar epithelium requires selective binding and endocytosis of inhaled nanomaterials. Further dissecting these incompletely understood mechanisms may lead to novel therapeutic approaches for patients with pulmonary inflammation and respiratory failure.
We welcome contributions in the form of Original Research, Brief Research Report, (Mini) Review, Perspective as well as Hypothesis and Theory primarily focusing on, but not limited to, the following topics in the context of acute lung injury and pulmonary inflammation:
• Dissecting the regulatory mechanisms of the endocytic machinery in alveolar epithelial and endothelial permeability and barrier integrity
• Analyses of polarized endocytic transport in the mechanisms of protein-rich pulmonary edema clearance in alveolar fluid balance
• Understanding the role of trafficking in interactions among the alveolar epithelium, endothelium and the extracellular matrix
• Establishing novel fully functional three dimensional lung model systems to study trafficking events
• Enhancing cell-type specific, super-selective pulmonary targeting using nanoparticles
Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic, no other organ has been as much in the focus of research as the lung. However, many other causes may also lead to inflammation and severe damage of the lung, potentially leading to life-threatening acute respiratory distress syndrome (ARDS). The loss of alveolar-capillary barrier integrity plays a pivotal role in the pathogenesis of respiratory inflammation and failure. Moreover, repair of the injured air-blood barrier is key for recovery. Endocytic and trafficking events in alveolar epithelial and endothelial cells, the major components of this barrier, as well as in neutrophils and macrophages, which predominantly regulate pulmonary inflammation, are centrally involved in both the emergence of and recovery from lung damage.
The primary goal of this Research Topic is to enhance our understanding regarding the role of endocytosis and trafficking in regulation of alveolar-capillary barrier integrity. Recent technological advances enable dissection of the precise lung cell-specific molecular patterns of these events in complex lung model systems. For example, recent evidence suggests that both entry and propagation of severe acute respiratory syndrome coronavirus 2 (SARS-COV-2), influenza virus and respiratory syncytial virus are mediated by spatiotemporally-specific epithelial endocytic processes. Furthermore, protein-rich pulmonary edema secondary to virus-induced lung damage is cleared from the alveolar space by well-defined endocytic processes that critically influence survival of patients with ARDS. Moreover, endothelial barrier integrity in the lung is maintained in part by adherens junction proteins, expression of which at the cell surface is tightly regulated by endocytic trafficking. Finally, uptake and intracellular processing of engineered nanoparticles during targeted delivery of drugs to the alveolar epithelium requires selective binding and endocytosis of inhaled nanomaterials. Further dissecting these incompletely understood mechanisms may lead to novel therapeutic approaches for patients with pulmonary inflammation and respiratory failure.
We welcome contributions in the form of Original Research, Brief Research Report, (Mini) Review, Perspective as well as Hypothesis and Theory primarily focusing on, but not limited to, the following topics in the context of acute lung injury and pulmonary inflammation:
• Dissecting the regulatory mechanisms of the endocytic machinery in alveolar epithelial and endothelial permeability and barrier integrity
• Analyses of polarized endocytic transport in the mechanisms of protein-rich pulmonary edema clearance in alveolar fluid balance
• Understanding the role of trafficking in interactions among the alveolar epithelium, endothelium and the extracellular matrix
• Establishing novel fully functional three dimensional lung model systems to study trafficking events
• Enhancing cell-type specific, super-selective pulmonary targeting using nanoparticles
