Within the lung, innate immune cells including epithelial cells, macrophages and dendritic cells (DC) comprise the first line defence against inhaled microbials, air pollutants and allergens. These cells play a major role in both inflammatory and repair responses in respiratory diseases, including infections, chronic obstructive lung disease (COPD), asthma, interstitial lung disease (ILD), and exacerbations of these diseases. Innate immune cell behaviour is dictated by cellular metabolism (catabolic and anabolic pathways) and metabolism of glucose, fatty acids and amino acids. Respiratory diseases have been implicated in altering these metabolic pathways leading to inadequate responses to insults and malfunctioning repair. A better understanding of the metabolic alterations in respiratory disease is essential to unravel mechanisms of disease pathogenesis and steer responses towards proper repair therapeutically.
Innate immune cellular behaviour is suggested to be altered in respiratory diseases, which may be mediated by alterations in cellular metabolism. For instance, mitochondrial metabolism was shown to be altered upon cigarette smoke exposure in lung epithelial cells, which affects their innate immune function. Furthermore, metabolic alteration may also affect the function of myeloid subsets in lung tissue and impair appropriate immune and repair responses to tackle invading pathogens and damaged cells/tissue. In this research topic, the aim is to highlight the differences in cellular metabolism in various chronic respiratory diseases, and whether/how these alterations offer potential therapeutic approaches or interventions targeting metabolic alterations to drive proper lung repair. Therefore, providing insight in differences in metabolism in different innate immune cell subsets in the lung, and the effects of metabolic alterations on lung repair and regeneration may be used to address this aim. Finally, novel methods or technology to detect (metabolic) alterations in innate immune cells in the lung are essential to make progress in this field.
This Research Topic welcomes the submission of original research, review or mini-review, short communications, and methods articles. In particular this topic will address, but is not limited to, the following aspects of Innate Immune Metabolism During Lung Repair:
• Differences in metabolism in different innate immune cell subsets in the lung, and the effects of metabolic alterations on lung repair and regeneration
• The effect of metabolic alteration on the function of myeloid subsets in lung tissue
• Differences in cellular metabolism in various chronic respiratory diseases
• Differences in metabolism in different innate immune cell subsets in the lung
• Metabolic alterations that offer potential therapeutic approaches or interventions to drive proper lung repair
• Novel methods or technology to detect (metabolic) alterations in innate immune cells in the lung
Topic Editor Dr. Barbro Melgerts received financial support from Boerhinger Ingelheim. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Within the lung, innate immune cells including epithelial cells, macrophages and dendritic cells (DC) comprise the first line defence against inhaled microbials, air pollutants and allergens. These cells play a major role in both inflammatory and repair responses in respiratory diseases, including infections, chronic obstructive lung disease (COPD), asthma, interstitial lung disease (ILD), and exacerbations of these diseases. Innate immune cell behaviour is dictated by cellular metabolism (catabolic and anabolic pathways) and metabolism of glucose, fatty acids and amino acids. Respiratory diseases have been implicated in altering these metabolic pathways leading to inadequate responses to insults and malfunctioning repair. A better understanding of the metabolic alterations in respiratory disease is essential to unravel mechanisms of disease pathogenesis and steer responses towards proper repair therapeutically.
Innate immune cellular behaviour is suggested to be altered in respiratory diseases, which may be mediated by alterations in cellular metabolism. For instance, mitochondrial metabolism was shown to be altered upon cigarette smoke exposure in lung epithelial cells, which affects their innate immune function. Furthermore, metabolic alteration may also affect the function of myeloid subsets in lung tissue and impair appropriate immune and repair responses to tackle invading pathogens and damaged cells/tissue. In this research topic, the aim is to highlight the differences in cellular metabolism in various chronic respiratory diseases, and whether/how these alterations offer potential therapeutic approaches or interventions targeting metabolic alterations to drive proper lung repair. Therefore, providing insight in differences in metabolism in different innate immune cell subsets in the lung, and the effects of metabolic alterations on lung repair and regeneration may be used to address this aim. Finally, novel methods or technology to detect (metabolic) alterations in innate immune cells in the lung are essential to make progress in this field.
This Research Topic welcomes the submission of original research, review or mini-review, short communications, and methods articles. In particular this topic will address, but is not limited to, the following aspects of Innate Immune Metabolism During Lung Repair:
• Differences in metabolism in different innate immune cell subsets in the lung, and the effects of metabolic alterations on lung repair and regeneration
• The effect of metabolic alteration on the function of myeloid subsets in lung tissue
• Differences in cellular metabolism in various chronic respiratory diseases
• Differences in metabolism in different innate immune cell subsets in the lung
• Metabolic alterations that offer potential therapeutic approaches or interventions to drive proper lung repair
• Novel methods or technology to detect (metabolic) alterations in innate immune cells in the lung
Topic Editor Dr. Barbro Melgerts received financial support from Boerhinger Ingelheim. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
