Severe asthma is a disease affecting about 5-10% of asthmatic patients, characterized by poor symptom control and frequent use of systemic corticosteroids. In order to reduce the short and long-term impact of systemic steroid therapy, several drugs have been developed to replace the steroid while maintaining control of the disease. The knowledge of pathogenetic mechanisms, phenotypes, and endotypes, allowed clinicians to use increasingly precise and personalized therapies to act on the individual causes of disease. However, although several phenotypes and their endotypes have been recognized, the mechanisms underlying the disease have not been fully elucidated. In recent years, a more in-depth analysis of the characteristics of patients suffering from this type of asthma has revealed a crucial role of the immune system, such as the reaction to contact with allergens, or the activation of immunity cascade with the liberation of cytokines and chemokines. Further analysis is also highlighting the role of the microbiome as a possible pathogenesis cofactor in the onset of severe asthma, but the exact contribution of the microbiome is still unclear. For several years now, two major endotypes of the disease have been known, which can be distinguished by the mechanisms underlying the inflammatory cascade: asthma type 2, involving type 2 T helper lymphoid cells, type 2 innate lymphoid cells (ILC2) and a series of cytokines (principally IL-5, IL-4, IL-13, IL-33, TSLP), and a type of asthma not type 2, when this type of inflammation is not present. The development of research in the field of microbiome and its relationship with the immune response could open up the way for understanding the pathogenesis of severe asthma and propose new therapeutic strategies both for asthma type 2 and non-type 2 which, at the moment, can’t benefit from many therapeutic approaches.
The aim of this Research Topic is to investigate the immune response, particularly innate immunity, and microbiome in severe asthma, evaluating the possible effects on the development of this disease and of potential pheno-endotypical differences. A deeper knowledge of these issues would allow us to reach a more and more personalized therapy for these patients, better targeting the mechanisms responsible for the pathology.
We welcome the submission of Original Research and Review article covering the following subtopics around severe asthma:
1) Innate immunity and inflammation: implications in severe asthma
2) Epithelial barrier dysfunction and impaired immune response
3) The role of the microbiome in bronchial homeostasis and implications in asthma development
4) Relationship between microbiome and immune response in the pathogenesis and potential treatment of asthma
5) The role of innate immunity in the onset of Non type 2 asthma
Topic Editor Dr. Choy is employed by Genentech. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Severe asthma is a disease affecting about 5-10% of asthmatic patients, characterized by poor symptom control and frequent use of systemic corticosteroids. In order to reduce the short and long-term impact of systemic steroid therapy, several drugs have been developed to replace the steroid while maintaining control of the disease. The knowledge of pathogenetic mechanisms, phenotypes, and endotypes, allowed clinicians to use increasingly precise and personalized therapies to act on the individual causes of disease. However, although several phenotypes and their endotypes have been recognized, the mechanisms underlying the disease have not been fully elucidated. In recent years, a more in-depth analysis of the characteristics of patients suffering from this type of asthma has revealed a crucial role of the immune system, such as the reaction to contact with allergens, or the activation of immunity cascade with the liberation of cytokines and chemokines. Further analysis is also highlighting the role of the microbiome as a possible pathogenesis cofactor in the onset of severe asthma, but the exact contribution of the microbiome is still unclear. For several years now, two major endotypes of the disease have been known, which can be distinguished by the mechanisms underlying the inflammatory cascade: asthma type 2, involving type 2 T helper lymphoid cells, type 2 innate lymphoid cells (ILC2) and a series of cytokines (principally IL-5, IL-4, IL-13, IL-33, TSLP), and a type of asthma not type 2, when this type of inflammation is not present. The development of research in the field of microbiome and its relationship with the immune response could open up the way for understanding the pathogenesis of severe asthma and propose new therapeutic strategies both for asthma type 2 and non-type 2 which, at the moment, can’t benefit from many therapeutic approaches.
The aim of this Research Topic is to investigate the immune response, particularly innate immunity, and microbiome in severe asthma, evaluating the possible effects on the development of this disease and of potential pheno-endotypical differences. A deeper knowledge of these issues would allow us to reach a more and more personalized therapy for these patients, better targeting the mechanisms responsible for the pathology.
We welcome the submission of Original Research and Review article covering the following subtopics around severe asthma:
1) Innate immunity and inflammation: implications in severe asthma
2) Epithelial barrier dysfunction and impaired immune response
3) The role of the microbiome in bronchial homeostasis and implications in asthma development
4) Relationship between microbiome and immune response in the pathogenesis and potential treatment of asthma
5) The role of innate immunity in the onset of Non type 2 asthma
Topic Editor Dr. Choy is employed by Genentech. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
