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J Allergy Clin Immunol. 2013 Jul;132(1):159-69. doi: 10.1016/j.jaci.2013.01.003. Epub 2013 Feb 10.

Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides.

Author information

1
Division of Asthma Research, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.

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.

PMID:
23403046
PMCID:
PMC6145803
DOI:
10.1016/j.jaci.2013.01.003
[Indexed for MEDLINE]
Free PMC Article

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