ArticleThe Journal of allergy and clinical immunology2013
Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides.
Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Household mold exposure and arthritis in older Chinese adults: evidence from the Chinese Longitudinal Healthy Longevity Survey (CLHLS).BMC geriatrics · 2026Article
- Association between indoor ventilation frequency and frailty among Chinese older adults.Frontiers in public health · 2025Article
- Defense Mechanisms of CottonInternational journal of molecular sciences · 2022Review
- Mold, Mycotoxins and a Dysregulated Immune System: A Combination of Concern?International journal of molecular sciences · 2021Review
- Assessment of the pulmonary adaptive immune response to Cladosporium cladosporioides infection using an experimental mouse model.Scientific reports · 2021Article
- Th17/IL-17 Axis Regulated by Airway Microbes Get Involved in the Development of Asthma.Current allergy and asthma reports · 2020Review
- The Composition of Fungal Communities in the Rumen of Gayals (Polish journal of microbiology · 2019Article
- Environmental exposures and mechanisms in allergy and asthma development.The Journal of clinical investigation · 2019Review
- Environment and Host-Genetic Determinants in Early Development of Allergic Asthma: Contribution of Fungi.Frontiers in immunology · 2019Review
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- C-Type Lectin Receptors in Asthma.Frontiers in immunology · 2018Review
- β-Glucan exacerbates allergic asthma independent of fungal sensitization and promotes steroid-resistant TThe Journal of allergy and clinical immunology · 2017Article
- Modulation of Human Immune Response by Fungal Biocontrol Agents.Frontiers in microbiology · 2017Review
- Fungal Exposure and Asthma: IgE and Non-IgE-Mediated Mechanisms.Current allergy and asthma reports · 2016Review
- Immune responses to airborne fungi and non-invasive airway diseases.Seminars in immunopathology · 2015Review
- Article
- Innate receptors and cellular defense against pulmonary infections.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIt is well accepted that mold exposure is a major contributor to the development of asthma, and beta-glucans are often used as a surrogate for mold exposure in the environment. Beta-glucans are an important component of mold spores and are recognized by the immune system by their receptor, Dectin-1. Cladosporium cladosporioides spores have a high beta-glucan content, but the beta-glucans are not available on the surface of live spores.
objectiveWe sought to determine whether altering the exposure of beta-glucans in C cladosporioides through heat killing could alter the immune response through binding to Dectin-1.
methodsIn a murine model of mold-induced asthma, mice were repeatedly exposed to either live or heat-killed C cladosporioides and the phenotype was determined by the measurement of airway hyperresponsiveness, airway inflammation, and cytokine production. Pro-inflammatory cytokines from dendritic cells were measured by using quantitative PCR and ELISA.
resultsLive C cladosporioides induced robust airway hyperresponsiveness, eosinophilia, and a predominately TH2 response, while heat-killed C cladosporioides induced a strong TH17 response and neutrophilic inflammation, but very mild airway hyperresponsiveness. Heat killing of C cladosporioides spores effectively exposed beta-glucans on the surface of the spores and increased binding to Dectin-1. In the absence of Dectin-1, heat-killed spores induced a predominantly TH2 response analogous to live spores. Furthermore, the production of TH17-skewing IL-6, IL-23, and TNF-α by dendritic cells in response to heat-killed C cladosporioides was dependent on Dectin-1.
conclusionsThe host immune response to C cladosporioides is dependent on the surface availability of beta-glucans rather than the total beta-glucan content.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.