Publication date: April 2018
Source:Journal of Allergy and Clinical Immunology, Volume 141, Issue 4
Author(s): Ubong Peters, Anne E. Dixon, Erick Forno
Information for Category 1 CME CreditCredit can now be obtained, free for a limited time, by reading the review articles in this issue. Please note the following instructions.Method of Physician Participation in Learning Process: The core material for these activities can be read in this issue of the Journal or online at the JACI Web site: www.jacionline.org. The accompanying tests may only be submitted online at www.jacionline.org. Fax or other copies will not be accepted.Date of Original Release: April 2018. Credit may be obtained for these courses until March 31, 2019.Copyright Statement: Copyright © 2018-2019. All rights reserved.Overall Purpose/Goal: To provide excellent reviews on key aspects of allergic disease to those who research, treat, or manage allergic disease.Target Audience: Physicians and researchers within the field of allergic disease.Accreditation/Provider Statements and Credit Designation: The American Academy of Allergy, Asthma & Immunology (AAAAI) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. The AAAAI designates this journal-based CME activity for a maximum of 1.00 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.List of Design Committee Members: Ubong Peters, PhD, Anne E. Dixon, MA, BM, BCh, and Erick Forno, MD, MPH (authors); Andrea Apter, MD, MA, MSc (editor)Disclosure of Significant Relationships with Relevant CommercialCompanies/Organizations: A. E. Dixon has received grants from the National Institutes of Health, the American Lung Association, and Pfizer and has received personal fees from Vitaeris. The rest of the authors declare that they have no relevant conflicts of interest. A. Apter (editor) declares that she has no relevant conflicts of interest.Activity Objectives:1. To understand the role that obesity plays as a risk factor for and disease modifier of asthma.2. To identify the mechanisms involved in asthma pathogenesis.3. To understand the evidence supporting lifestyle changes in influencing disease progression.4. To identify the clinical characteristics of obese asthma in children and adults.Recognition of Commercial Support: This CME activity has not received external commercial support.List of CME Exam Authors: Gagandeep Cheema, MD, Erica Ridley, MD, Eliane Abou-Jaoude, MD, and Christian Nageotte, MD.Disclosure of Significant Relationships with Relevant CommercialCompanies/Organizations: The exam authors disclosed no relevant financial relationships.Obesity is a vast public health problem and both a major risk factor and disease modifier for asthma in children and adults. Obese subjects have increased asthma risk, and obese asthmatic patients have more symptoms, more frequent and severe exacerbations, reduced response to several asthma medications, and decreased quality of life. Obese asthma is a complex syndrome, including different phenotypes of disease that are just beginning to be understood. We examine the epidemiology and characteristics of this syndrome in children and adults, as well as the changes in lung function seen in each age group. We then discuss the better recognized factors and mechanisms involved in disease pathogenesis, focusing particularly on diet and nutrients, the microbiome, inflammatory and metabolic dysregulation, and the genetics/genomics of obese asthma. Finally, we describe current evidence on the effect of weight loss and mention some important future directions for research in the field.
https://ift.tt/2GX4qVL
Publication date: Available online 4 April 2018
Source:Journal of Allergy and Clinical Immunology
Author(s): Antonia Fettelschoss-Gabriel, Victoria Fettelschoss, Franziska Thoms, Christoph Giese, Michelle Daniel, Florian Olomski, Jivko Kamarachev, Katharina Birkmann, Maya Bühler, Martin Kummer, Andris Zeltins, Eliane Marti, Thomas M. Kündig, Martin F. Bachmann
BackgroundInsect-bite hypersensitivity is the most common allergic dermatitis in horses. Excoriated skin lesions are typical symptoms of this seasonal and refractory chronic disease. On a cellular level, the skin lesions are characterized by massive eosinophil infiltration caused by an underlying allergic response.ObjectiveTo target these cells and treat disease, we developed a therapeutic vaccine against equine IL-5 (eIL-5), the master regulator of eosinophils.MethodsThe vaccine consisted of eIL-5 covalently linked to a virus-like particle derived from cucumber mosaic virus containing the tetanus toxoid universal T-cell epitope tt830-843 (CMVTT). Thirty-four Icelandic horses were recruited and immunized with 400 μg of eIL-5–CMVTT formulated in PBS without adjuvant (19 horses) or PBS alone (15 horses).ResultsThe vaccine was well tolerated and did not reveal any safety concerns but was able to induce anti–eIL-5 autoantibody titers in 17 of 19 horses. This resulted in a statistically significant reduction in clinical lesion scores when compared with previous season levels, as well as levels in placebo-treated horses. Protection required a minimal threshold of anti–eIL-5 antibodies. Clinical improvement by disease scoring showed that 47% and 21% of vaccinated horses reached 50% and 75% improvement, respectively. In the placebo group no horse reached 75% improvement, and only 13% reached 50% improvement.ConclusionOur therapeutic vaccine inducing autoantibodies against self IL-5 brings biologics to horses, is the first successful immunotherapeutic approach targeting a chronic disease in horses, and might facilitate development of a similar vaccine against IL-5 in human subjects.
Publication date: April 2018
Source:Journal of Allergy and Clinical Immunology, Volume 141, Issue 4
https://ift.tt/2GTdYBp
Resident microbial communities likely modify risk for allergic disorders, including food allergy. We review epidemiologic studies linking microbial exposures to food allergy risk and discuss the mechanisms by which the microbiome may modulate oral tolerance. We additionally address ongoing translational efforts in human microbiome studies.
Epidemiologic studies and murine models support that altered microbial exposures and colonization in early life modify food allergy risk. Differential microbiota confer protection or susceptibility to food allergy by modulating the regulatory tone of the mucosal immune system. Recent efforts are focused on the identification of bacterial strains necessary for oral tolerance in human and microbial-based clinical trials.
Early childhood appears to be critical for the colonization of a diverse microbiota necessary for the induction and maintenance of oral tolerance. Identification and functional evaluation of protective commensal microbes will inform strategies for the prevention and treatment of food allergy.
