Letter to the EditorInterferon-induced epithelial response to rhinovirus 16 in asthma relates to inflammation and FEV1
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2021, Journal of Allergy and Clinical ImmunologyCitation Excerpt :The baseline characteristics of the patients with asthma and healthy controls who were involved in this study are provided in Table I. The inclusion and exclusion criteria for patients with mild asthma (from the RESOLVE and MATERIAL trials) are described elaborately16 in the Methods section of the Online Repository (available at www.jacionline.org). Patients with severe asthma (from the TASMA trial) fulfilling the World Health Organization or modified innovative medicines initiative criteria of severe refractory asthma were included.17,18
Human T<inf>H</inf>1 and T<inf>H</inf>2 cells targeting rhinovirus and allergen coordinately promote allergic asthma
2020, Journal of Allergy and Clinical ImmunologyCitation Excerpt :However, different mechanisms may regulate the production of IFNs in the airways. Several newer studies indicate that IFN responses are not deficient at the epithelial barrier in asthmatic subjects infected with RV, or in those experiencing cold symptoms.27,30,67 One report suggests that mast cells, which are enriched in the allergic airways, may contribute to IFN production when type 2 inflammation is present.
Exacerbation-Prone Asthma
2020, Journal of Allergy and Clinical Immunology: In PracticeCitation Excerpt :However, some experimental inoculation studies41,42 and clinical studies43,44 have found similar viral shedding in patients with asthma compared with controls without asthma, suggesting that antiviral responses in asthma vary with disease severity, control, or phenotype (eg, atopic vs nonatopic). Finally, there is evidence that the timing and magnitude of IFN responses are important; brisk responses during the first hours of infection could inhibit viral replication and preclude severe illness, whereas weak initial responses could lead to greater replication and induction of high-level IFN that contributes to symptoms of illness.45,46 In keeping with the hygiene hypothesis, exposure to microbial organisms (other than viruses) in the environment, or as part of the microbiota on our skin and mucosal surfaces, can influence immune responses to viruses and allergens.
IL-33 drives influenza-induced asthma exacerbations by halting innate and adaptive antiviral immunity
2019, Journal of Allergy and Clinical ImmunologyCitation Excerpt :Details on collection and processing of other murine samples are provided in the Methods section in this article's Online Repository. Primary bronchial epithelial cells (PBECs) were obtained from 17 atopic patients with mild asthma who were steroid naive and 4 nonatopic, nonasthmatic healthy subjects without a recent infection and no serum-neutralizing antibodies to rhinovirus-16 (RV16) at screening (≤1/4), before and 6 days after RV16 exposure (Sabogal Pineros et al27; Ravi et al28). Clinical characteristics of asthmatic patients and healthy subjects recruited by using strict inclusion and exclusion criteria are reported in Table E1 in this article's Online Repository at www.jacionline.org.
Supported by the Stichting Astma Bestrijding (project 2013_009) and Netherlands Asthma Foundation (currently Lung Foundation; projects 3.2.10.069, 3.2.07.012, and 3.2.06.031) and GlaxoSmithKline (CRT 114696).
Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.