The adaptor molecule MyD88: an inhibitory pathway of the allergic response induced by Aspergillus fumigatus spores

Author:

Percier-Lehebel P; De Prins S; Tima HG; Huygen K; Romano M; Denis O

Author address:

Scientific Institute of Public Health, Brussels, Belgium

Full conference title:

European Academy of Allergy and Clinical Immunology Congress 2017

Abstract:

Introduction: Aspergillus fumigatus is one of the most ubiquitous of the airborne saprophytic fungi, found both outdoors and indoors. Every day, humans inhale thousands of Aspergillus fumigatus conidia. In immunocompetent host, these conidia are eliminated by the innate immune system and a protective inflammation through the generation of Th1/Th17 responses. But in immuno-compromised hosts, Aspergillus fumigatus can induce serious diseases like aspergillosis. However, this aggressive fungi species can also activate detrimental Th2 responses in the lungs leading to the development of an allergic inflammation in such hosts.

Objectives: The early events inducing the allergic inflammation induced by Aspergillus fumigatus are actually not defined. The immune activating properties of this fungus species have been investigated in an asthma murine model to determine which receptor, signaling pathway are activated by conidia and identify which cytokines are crucial in this model.

Results: A model of lung allergic inflammation based on the transfer of dendritic cells pulsed in vitro with Aspergillus fumigatus was developed. Bone marrow-derived dendritic cells (BMDCs) from wild type or deficient mice were stimulated in vitro with Aspergillus fumigatus conidia and then transferred into wild type mice by intranasal administration. Fourteen days after the transfer, all mice were challenged with conidia intra-nasally and the lung inflammations were analysed three days later. This fungus species induced a strong lung Th2 response with a high recruitment of eosinophils in broncho-alveolar lavages and an increase of Th2 cytokine mRNA in lung homogenate. The transfer of BMDCs deficient for the expression of MyD88 induced a worsening of the allergic lung inflammation, which is specific of the Aspergillus fumigatus species.

Conclusions: These results indicate that the MyD88 pathway on BMDCs is able to control the allergic response generated by A. fumigatus via the recognition of compounds on Aspergillus fumigatus conidia.

Abstract Number: 1650

Conference Year: 2017

Link Conference abstract: 

EAACI 2017

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