About this Research Topic
Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD) is a clinical syndrome characterized by nasal polyposis, asthma, and intolerance to aspirin /NSAID. It affects approximately 15% cases of severe asthma, 10% of nasal polyps and 9% of rhinosinusitis. NERD results in associated asthma exacerbation, oral corticosteroids bursts, corticosteroid-dependent disease, and multiple endoscopic sinus surgeries.
NERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. The release by mast cells, eosinophils, platelets cause the epithelial release of IL-33 and TSLP and these cytokines activate innate lymphoid cell type 2 (ILC2). The inflammatory response is driven by multiple factors. Mast cell activation and interaction between platelets and granulocytes lead to overproduction of CysLT and severe eosinophilic inflammation. Defective epithelial barrier and lung dysbiosis support the activation of inflammatory pathways and contributes increase symptoms.
Patients with NERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives.
Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with NERD. The most important strategies for treating NERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. NERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential.
This Research Topic aims to define the inflammatory response driven by multiple factors such as epigenetic reprogramming, transcriptional genes, lung dysbiosis, imbalance in eicosanoid levels, defective epithelial barrier, nasal and lung dysbiosis, which will unite all the information for a better understand of the disease.
All forms of contribution that are currently accepted by Frontiers in Allergy are welcome.
Specific topics may include, but are not limited to, the following:
• Defining AERD phenotype
• Define what characterized patients should have to treatment monoclonal antibody, aspirin desensitization or both
• Defective epithelial barrier and AERD
• Microbiota and AERD
• Gustatory disfunction and AERD
• Severe asthma and AERD
• Monoclonal antibody vs aspirin desensitization
NERD is characterized by an imbalance in eicosanoid levels, especially CysLTs, PDG and PGE2. The release by mast cells, eosinophils, platelets cause the epithelial release of IL-33 and TSLP and these cytokines activate innate lymphoid cell type 2 (ILC2). The inflammatory response is driven by multiple factors. Mast cell activation and interaction between platelets and granulocytes lead to overproduction of CysLT and severe eosinophilic inflammation. Defective epithelial barrier and lung dysbiosis support the activation of inflammatory pathways and contributes increase symptoms.
Patients with NERD present nasal symptoms (congestion, hyposmia/anosmia, nasal discharge) and lower airways symptoms (cough, sneezing, shortness of breath, chest tightness), anosmia, severe hyposmia as well as severe asthma which impacts the quality of life in this disease and leads to safety concerns in patients daily lives.
Despite the variety of treatment strategies, the likelihood of recurrence of symptoms is high in patients with NERD. The most important strategies for treating NERD are listed as following: drug therapies, aspirin desensitization, monoclonal antibodies and other therapies associated. NERD treatment remains a major challenge in the current situation. Selecting the appropriate patient for aspirin desensitization, monoclonal antibodies or both is essential.
This Research Topic aims to define the inflammatory response driven by multiple factors such as epigenetic reprogramming, transcriptional genes, lung dysbiosis, imbalance in eicosanoid levels, defective epithelial barrier, nasal and lung dysbiosis, which will unite all the information for a better understand of the disease.
All forms of contribution that are currently accepted by Frontiers in Allergy are welcome.
Specific topics may include, but are not limited to, the following:
• Defining AERD phenotype
• Define what characterized patients should have to treatment monoclonal antibody, aspirin desensitization or both
• Defective epithelial barrier and AERD
• Microbiota and AERD
• Gustatory disfunction and AERD
• Severe asthma and AERD
• Monoclonal antibody vs aspirin desensitization
Keywords: Aspirin-exacerbated Respiratory Disease, NERD, epigenetic reprogramming, aspirin desensitization, monoclonal antibody
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
