Allergic airway inflammation is an abnormally exacerbated reaction towards common environmental factors, such as pollen grains or dust mites. It involves several cell types including airway epithelial cells, Th2 cells, mast cells, eosinophils and basophils. Th2-related cytokines IL4, IL-5, IL-9 and IL-13; and the production of allergen-specific IgE also contribute to this inflammation. When allergic airway inflammation becomes chronic, it leads to the development of asthma. At an early age, allergic sensitization towards allergenic proteins takes place in susceptible individuals. Thus, protein-derived allergens have been the focus of research regarding allergic airway inflammation. However, allergens do not arrive in the airways alone. Their delivery occurs exclusively in particles, which consist of a complex mixture of chemically different molecules, including lipids. Hence, allergic sensitization is a multifactorial process that is not only regulated by the intrinsic biological activity (i.e. protease activity) of the allergens but also by bioactive lipids. These lipids are either associated to the allergens as ligands, as a component of the allergenic particles, or are derived from microorganisms present on the allergen source.
By definition, lipids are hydrophobic or small amphipathic molecules, and have been recently classified into eight well-defined categories (Fatty acyls, glycerolipids, glycerophospholipids, sphingolipids, sterol lipids, prenol lipids saccharolipids and polyketides). There is now a growing body of evidence indicating that certain members of the categories comprising fatty acids, glycerolipids, glycerophospholipids, sphingolipids, and saccharolipids; can target different cell populations of the immune system; namely: airway epithelial cells, dendritic cells, NKT and ?d-T cells. Therefore, it is likely that these molecules play key roles in the dynamics (sensitization-chronification-exacerbation) of allergic airway inflammation. However, the precise structure-activity relationship driving the inflammatory response towards an allergic phenotype remains poorly understood.
This Research Topic aims to provide a comprehensive overview of the role of lipids in the dynamics of allergic airway inflammation, with an emphasis on the structure-activity relationship. We welcome the submission of Original Research, Technology Report, Review, Mini Review, Perspective and Clinical Trial articles covering the following topics, but not limited to:
1. Structural studies on lipids derived from allergen sources.
2. NKT and ?d-T cell activation by glycerolipids, glycerophospholipids and sphingolipids.
3. Priming of antigen presenting cells (e.g. DCs and macrophages) towards a Th2-inducing phenotype in allergic airway inflammation.
4. Direct activation of effector cells during allergic inflammatory processes, such as mast cells, basophils and eosinophils.
5. Lipids derived from microorganisms present in allergen sources.
6. Therapeutic uses of lipids.
7. Environmental influence on lipid pollen and allerginicity.
8. Monitoring of airborne immunogenic compounds associated with allergic asthma.
Allergic airway inflammation is an abnormally exacerbated reaction towards common environmental factors, such as pollen grains or dust mites. It involves several cell types including airway epithelial cells, Th2 cells, mast cells, eosinophils and basophils. Th2-related cytokines IL4, IL-5, IL-9 and IL-13; and the production of allergen-specific IgE also contribute to this inflammation. When allergic airway inflammation becomes chronic, it leads to the development of asthma. At an early age, allergic sensitization towards allergenic proteins takes place in susceptible individuals. Thus, protein-derived allergens have been the focus of research regarding allergic airway inflammation. However, allergens do not arrive in the airways alone. Their delivery occurs exclusively in particles, which consist of a complex mixture of chemically different molecules, including lipids. Hence, allergic sensitization is a multifactorial process that is not only regulated by the intrinsic biological activity (i.e. protease activity) of the allergens but also by bioactive lipids. These lipids are either associated to the allergens as ligands, as a component of the allergenic particles, or are derived from microorganisms present on the allergen source.
By definition, lipids are hydrophobic or small amphipathic molecules, and have been recently classified into eight well-defined categories (Fatty acyls, glycerolipids, glycerophospholipids, sphingolipids, sterol lipids, prenol lipids saccharolipids and polyketides). There is now a growing body of evidence indicating that certain members of the categories comprising fatty acids, glycerolipids, glycerophospholipids, sphingolipids, and saccharolipids; can target different cell populations of the immune system; namely: airway epithelial cells, dendritic cells, NKT and ?d-T cells. Therefore, it is likely that these molecules play key roles in the dynamics (sensitization-chronification-exacerbation) of allergic airway inflammation. However, the precise structure-activity relationship driving the inflammatory response towards an allergic phenotype remains poorly understood.
This Research Topic aims to provide a comprehensive overview of the role of lipids in the dynamics of allergic airway inflammation, with an emphasis on the structure-activity relationship. We welcome the submission of Original Research, Technology Report, Review, Mini Review, Perspective and Clinical Trial articles covering the following topics, but not limited to:
1. Structural studies on lipids derived from allergen sources.
2. NKT and ?d-T cell activation by glycerolipids, glycerophospholipids and sphingolipids.
3. Priming of antigen presenting cells (e.g. DCs and macrophages) towards a Th2-inducing phenotype in allergic airway inflammation.
4. Direct activation of effector cells during allergic inflammatory processes, such as mast cells, basophils and eosinophils.
5. Lipids derived from microorganisms present in allergen sources.
6. Therapeutic uses of lipids.
7. Environmental influence on lipid pollen and allerginicity.
8. Monitoring of airborne immunogenic compounds associated with allergic asthma.
