Abstract
The mechanisms explaining multimorbidity between asthma, dermatitis and rhinitis (allergic multimorbidity) are not well known. We investigated these mechanisms and their specificity in distinct cell types by means of an interactome-based analysis of expression data. Genes associated to the diseases were identified using data mining approaches, and their multimorbidity mechanisms in distinct cell types were characterized by means of an in silico analysis of the topology of the human interactome. We characterized specific pathomechanisms for multimorbidities between asthma, dermatitis and rhinitis for distinct emergent non-eosinophilic cell types. We observed differential roles for cytokine signaling, TLR-mediated signaling and metabolic pathways for multimorbidities across distinct cell types. Furthermore, we also identified individual genes potentially associated to multimorbidity mechanisms. Our results support the existence of differentiated multimorbidity mechanisms between asthma, dermatitis and rhinitis at cell type level, as well as mechanisms common to distinct cell types. These results will help understanding the biology underlying allergic multimorbidity, assisting in the design of new clinical studies.
Highlights
Mapping diseases onto molecular interaction networks, has contributed to the elucidation of disease mechanisms and the identification of new disease-associated genes [1, 2]
We identified individual genes potentially associated to multimorbidity mechanisms
Our results support the existence of differentiated multimorbidity mechanisms between asthma, dermatitis and rhinitis at cell type level, as well as mechanisms common to distinct
Summary
Mapping diseases onto molecular interaction networks (such as the protein-protein interaction network, known as the interactome), has contributed to the elucidation of disease mechanisms and the identification of new disease-associated genes [1, 2]. Disease-associated genes are usually tissue-specific and their interaction patterns with other genes change in diseased tissues as compared to healthy ones [9]. These observations make elucidating the context-specific role of genes in pathophysiological processes challenging [10, 11]. The mechanisms explaining multimorbidity between asthma, dermatitis and rhinitis (allergic multimorbidity) are not well known. We investigated these mechanisms and their specificity in distinct cell types by means of an interactome-based analysis of expression data
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