A5080646352- Asthma and respiratory diseases
- Allergic Rhinitis and Sensitization
- Diabetes and associated disorders
- Disaster Response and Management
- Respiratory and Cough-Related Research
- IL-33, ST2, and ILC Pathways
- SARS-CoV-2 and COVID-19 Research
- Food Allergy and Anaphylaxis Research
- COVID-19 Clinical Research Studies
- Long-Term Effects of COVID-19
- Inflammatory mediators and NSAID effects
- COVID-19 and Mental Health
- Cell Adhesion Molecules Research
- COVID-19 epidemiological studies
- COVID-19 Impact on Reproduction
- Kawasaki Disease and Coronary Complications
- Eosinophilic Esophagitis
- Protein Hydrolysis and Bioactive Peptides
- Intensive Care Unit Cognitive Disorders
- Pediatric health and respiratory diseases
- Systemic Lupus Erythematosus Research
- Transgenic Plants and Applications
- Monoclonal and Polyclonal Antibodies Research
- Respiratory viral infections research
- Respiratory Support and Mechanisms
Icahn School of Medicine at Mount Sinai
2020-2024
National Institute of Allergy and Infectious Diseases
2018-2021
National Institutes of Health
2018-2021
Centre for Inflammation Research
2018
Centre for Immunity, Infection and Evolution
2018
University of Edinburgh
2018
Food allergy is caused by allergen-specific immunoglobulin E (IgE) antibodies, but little known about the B cell memory of persistent IgE responses. Here, we describe, in human pediatric peanut allergy, a population CD23 + IgG1 cells arising type 2 immune responses that contain high-affinity peanut-specific clones and generate IgE-producing upon activation. The frequency correlated with circulating concentrations children allergy. A corresponding “type 2–marked” was identified single-cell...
Allergens elicit host production of mediators acting on G-protein-coupled receptors to regulate airway tone. Among these is prostaglandin E2 (PGE2), which, in addition its role as a bronchodilator, has anti-inflammatory actions. Some patients with asthma develop bronchospasm after the ingestion aspirin and other nonsteroidal drugs, disorder termed aspirin-exacerbated respiratory disease. This condition may result part from abnormal dependence bronchoprotective actions PGE2.We sought...
Abstract The hallmark features of allergic asthma are type 2 (eosinophilic) inflammation and airways hyperresponsiveness (AHR). Although these often comanifest in mouse lungs vivo, we demonstrate this study that the serine protease Alp1 from ubiquitous mold allergen, Aspergillus fumigatus, can induce AHR mice unable to generate eosinophilic inflammation. Strikingly, induced devoid protease-activated receptor 2/F2 trypsin-like 1 (PAR2/F2RL1), a expressed lung epithelium is critical for...
Abstract Fibroproliferative diseases affect a significant proportion of the world's population. Despite this, core mechanisms driving organ fibrosis diverse etiologies remain ill defined. Recent studies suggest that integrin‐alpha V serves as master driver in multiple organs. Although contribute to progression fibrosis, TGF‐β and IL‐13 have emerged central mediators during type 1/type 17, 2 polarized inflammatory responses, respectively. To investigate if interactions or signaling is...
Eosinophils in the nasal mucosa are an elemental feature of allergic rhinitis.
Respiratory virus infections can have long-term effects on lung function that persist even after the acute responses resolved. Numerous studies linked severe early childhood infection with respiratory syncytial (RSV) to development of wheezing and asthma, although underlying mechanisms connecting these observations remain unclear. Here, we examine airway hyperresponsiveness (AHR) develops in wild-type mice recovery from symptomatic but sublethal natural rodent pathogen, pneumonia (PVM). We...
Chronic inhalation of fungi and fungal components has been linked to the development respiratory disorders, although their role with respect pathogenesis acute virus infection remains unclear. Here, we evaluate inflammatory pathology induced by repetitive administration a filtrate ubiquitous fungus, Alternaria alternata, its impact on susceptibility influenza A. We showed previously that alternata at nasal mucosae resulted in increased an otherwise sublethal inoculum A wild-type mice. Here...