Respiratory virus and bacterial infections are the main cause of allergic asthma exacerbation in children and adults causing many hospitalizations worldwide. Type I interferons are a family of cytokines that include IFN-alpha and IFN-beta that were discovered more than 50 years ago. They are immediately induced following recognition of virus and bacterial-derived intracellular components like dsRNA, ssRNA, viral glycoproteins, or CpG-DNA by host pattern recognition receptors (PRRs). Every cell type expresses IFNAR1/INFAR2 receptors thus allowing a generalized antiviral activity of Type I interferons resulting in the inhibition of viral replication in infected cells and preventing viral spread in non-infected cells. Type I interferons also regulate the immune responses by activation of both innate and adaptive immune responses at the site of infection. By contrast, Type III interferon (IFN-lambda) has been discovered more recently. Although it has similar downstream molecular signaling, the IFN-Lambda receptor is expressed in selected types of cells like epithelial cells, resulting in a more specific antiviral immune response at the site of virus and bacteria entry. These findings have important implications for our understanding of asthma pathogenesis and exacerbations and in the design of novel therapeutic approaches.
It has been described that allergic asthma is associated with a defect in IFN type I production thus limiting the antiviral immune responses in this disease especially in children. Since type I interferons have a short half-life time, more research evidence is needed to analyze the reason and the type of this deficiency. The role of IFN-type III in asthma is less well understood. The role of IFN type III in respiratory infections needs further investigation with a focus on IFN Type III receptor regulation. Further analysis is required to understand the redundant and not redundant antiviral and antibacterial function of Type I and Type III Interferons in allergic asthma, focusing on the differential expression of their receptor during and after exacerbation of the disease. The following four aims should keep in focus the regulation of the immune responses following IFN-type I and Type III deficiency.
1) Interferons are potent effectors whose administration could lead to cytotoxic-generalized effects. It is thus important to exactly analyze the time frame of the IFN type I deficiency and the potential consequences of Interferon administration in allergic asthma especially in children and in the population in general.
2) In the case of an Interferon Type I deficiency, establish the role of IFN-Type III considering the selected cellular expression of its receptor. Thus defining the cellular and tissue distribution of the IFN-lambda receptor would be relevant.
3) To define the differential effects of Type I and Type III on the immune responses in healthy and asthmatic subjects.
4) Discussion of potential new therapeutic approaches in respiratory infections and their association with asthma based on the possibility to overcome the viruses immunescape targeting of IFNs.
In this Research Topic, we welcome authors to submit Original Research, Review, and Mini Review articles focusing on, but not limited to, the above topics.
Topic Editor Prof. Johnston is the author on patents relating to the use of inhaled type I and type III interferons in the treatment of exacerbations of respiratory disease
Respiratory virus and bacterial infections are the main cause of allergic asthma exacerbation in children and adults causing many hospitalizations worldwide. Type I interferons are a family of cytokines that include IFN-alpha and IFN-beta that were discovered more than 50 years ago. They are immediately induced following recognition of virus and bacterial-derived intracellular components like dsRNA, ssRNA, viral glycoproteins, or CpG-DNA by host pattern recognition receptors (PRRs). Every cell type expresses IFNAR1/INFAR2 receptors thus allowing a generalized antiviral activity of Type I interferons resulting in the inhibition of viral replication in infected cells and preventing viral spread in non-infected cells. Type I interferons also regulate the immune responses by activation of both innate and adaptive immune responses at the site of infection. By contrast, Type III interferon (IFN-lambda) has been discovered more recently. Although it has similar downstream molecular signaling, the IFN-Lambda receptor is expressed in selected types of cells like epithelial cells, resulting in a more specific antiviral immune response at the site of virus and bacteria entry. These findings have important implications for our understanding of asthma pathogenesis and exacerbations and in the design of novel therapeutic approaches.
It has been described that allergic asthma is associated with a defect in IFN type I production thus limiting the antiviral immune responses in this disease especially in children. Since type I interferons have a short half-life time, more research evidence is needed to analyze the reason and the type of this deficiency. The role of IFN-type III in asthma is less well understood. The role of IFN type III in respiratory infections needs further investigation with a focus on IFN Type III receptor regulation. Further analysis is required to understand the redundant and not redundant antiviral and antibacterial function of Type I and Type III Interferons in allergic asthma, focusing on the differential expression of their receptor during and after exacerbation of the disease. The following four aims should keep in focus the regulation of the immune responses following IFN-type I and Type III deficiency.
1) Interferons are potent effectors whose administration could lead to cytotoxic-generalized effects. It is thus important to exactly analyze the time frame of the IFN type I deficiency and the potential consequences of Interferon administration in allergic asthma especially in children and in the population in general.
2) In the case of an Interferon Type I deficiency, establish the role of IFN-Type III considering the selected cellular expression of its receptor. Thus defining the cellular and tissue distribution of the IFN-lambda receptor would be relevant.
3) To define the differential effects of Type I and Type III on the immune responses in healthy and asthmatic subjects.
4) Discussion of potential new therapeutic approaches in respiratory infections and their association with asthma based on the possibility to overcome the viruses immunescape targeting of IFNs.
In this Research Topic, we welcome authors to submit Original Research, Review, and Mini Review articles focusing on, but not limited to, the above topics.
Topic Editor Prof. Johnston is the author on patents relating to the use of inhaled type I and type III interferons in the treatment of exacerbations of respiratory disease
