Background: Flour is still one of the most common causes of occupational asthma worldwide. Thus far, little is known about the relevant allergens causing baker's asthma. Therefore the reliability of current diagnostic procedures is insufficient. Only few of the suspected causative wheat allergens have been hitherto characterized on the molecular level.
Objective: The aim was to identify and characterize unknown wheat allergens related to baker's asthma to improve the reliability of diagnostic procedures.
Methods: A wheat pJuFo cDNA phage display library was created and screened for IgE binding to wheat proteins with pooled sera from patients with baker's asthma. After identifying an alphabeta-gliadin, the frequency of sensitization was investigated by means of ELISA screening of 153 bakers' sera with the recombinant alphabeta-gliadin. Furthermore, the allergenicity of native total gliadin (alphabeta, gamma, omega) was analyzed by means of ImmunoCAP.
Results: One cDNA clone was identified as an alphabeta-gliadin. Serum IgE antibodies to the recombinant allergen were found in 12% of bakers with occupational asthma. Of the asthmatic bakers, 33% showed sensitization to native total gliadin; 4% of them had negative results on routine IgE testing with wheat extract.
Conclusions: Gliadins represent a newly discovered family of inhalable allergens in baker's asthma. This finding demonstrates that water-insoluble proteins might also represent causative allergens.
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http://dx.doi.org/10.1016/j.jaci.2007.09.051 | DOI Listing |
Nat Commun
January 2025
Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester, United Kingdom.
Fungal spores are abundant in the environment and a major cause of asthma. Originally characterised as a type 2 inflammatory disease, allergic airway inflammation that underpins asthma can also involve type 17 inflammation, which can exacerbate disease causing failure of treatments tailored to inhibit type 2 factors. However, the mechanisms that determine the host response to fungi, which can trigger both type 2 and type 17 inflammation in allergic airway disease, remain unclear.
View Article and Find Full Text PDFHawaii J Health Soc Welf
January 2025
Retired, Research Statistician Hawai'i Department of Health, Adjunct Assistant Professor, University of Hawai'i, Office of Public Health Studies, Honolulu, HI.
Information on companion animals in Hawai'i is lacking. The Hawai'i Department of Health's Hawai'i Health Survey, collected data on adults and households by telephone interview. National estimates of companion animals range from 50-67%.
View Article and Find Full Text PDFCurr Allergy Asthma Rep
December 2024
Laboratorios INMUNOTEK, Madrid, Spain.
We have read with great interest the recent review published by Dr. Ebo and collaborators on cannabis allergy. It highlights the difficulties in getting a valid diagnosis because some patients do not admit its consumption, which may not be legalized, there are no commercial extracts and there are problems in cutaneous tests interpretation due to cross-reactivity with other related allergens.
View Article and Find Full Text PDFSci Immunol
December 2024
Inflammation and Innate Immunity Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, MD 20892, USA.
Severity of COVID-19 is affected by multiple factors; however, it is not understood how the inflammatory milieu of the lung at the time of SARS-CoV-2 exposure affects the control of viral replication. Here, we demonstrate that immune events in the mouse lung closely preceding SARS-CoV-2 infection affect viral control and identify innate immune pathways that limit viral replication. Pulmonary inflammatory stimuli including resolved, antecedent respiratory infections with or influenza, ongoing pulmonary infection, ovalbumin/alum-induced asthma, or airway administration of TLR ligands and recombinant cytokines all establish an antiviral state in the lung that restricts SARS-CoV-2 replication.
View Article and Find Full Text PDFCommun Med (Lond)
November 2024
Department of Biochemistry and Pharmacology, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Parkville, VIC, Australia.
Background: Diagnosing complex illnesses like Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is complicated due to the diverse symptomology and presence of comorbid conditions. ME/CFS patients often present with multiple health issues, therefore, incorporating comorbidities into research can provide a more accurate understanding of the condition's symptomatology and severity, to better reflect real-life patient experiences.
Methods: We performed association studies and machine learning on 1194 ME/CFS individuals with blood plasma nuclear magnetic resonance (NMR) metabolomics profiles, and seven exclusive comorbid cohorts: hypertension (n = 13,559), depression (n = 2522), asthma (n = 6406), irritable bowel syndrome (n = 859), hay fever (n = 3025), hypothyroidism (n = 1226), migraine (n = 1551) and a non-diseased control group (n = 53,009).
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