Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides - 27/06/13
Abstract |
Background |
It 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.
Objective |
We 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.
Methods |
In 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.
Results |
Live 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.
Conclusions |
The host immune response to C cladosporioides is dependent on the surface availability of beta-glucans rather than the total beta-glucan content.
Le texte complet de cet article est disponible en PDF.Key words : Mold, Cladosporium cladosporioides, beta-glucans, asthma, Dectin-1
Abbreviations used : AHR, BALF, BMDCs
Plan
| This work was supported by NIAID grant no. 2U19AI70235-06 (to G.K.K.H.), NHBLI grant no. F30 HL103087 (to R.A.M.C.), and NIEHS grant no. T32 E5010956 (to E.B.B.). |
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| Disclosure of potential conflict of interest: R. A. Mintz-Cole has been supported by a Ruth L. Kirschstein NRSA Individual Fellowship. T. Reponen has received one or more grants from or has one or more grants pending with the US HUD (contract from the Centers for Disease Control and Prevention). G. K. Khurana Hershey has received one or more grants from or has one or more grants pending with the National Institutes of Health. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 132 - N° 1
P. 159 - juillet 2013 Retour au numéro
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