ArticlePloS one2011
Dual organism transcriptomics of airway epithelial cells interacting with conidia of Aspergillus fumigatus.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 73 citations in OpenAlex.
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- Accelerating the understanding ofCurrent research in microbial sciences · 2024Review
- Novel Treatment Approach for Aspergilloses by Targeting Germination.Journal of fungi (Basel, Switzerland) · 2022Review
- Respiratory Epithelial Cells: More Than Just a Physical Barrier to Fungal Infections.Journal of fungi (Basel, Switzerland) · 2022Review
- ClinicalJournal of fungi (Basel, Switzerland) · 2022Review
- Novel Insights intoJournal of fungi (Basel, Switzerland) · 2022Review
- Expression of immune response genes in human corneal epithelial cells interacting with Aspergillus flavus conidia.BMC genomics · 2022Article
- Extensive non-coding sequence divergence between the major human pathogenFrontiers in fungal biology · 2022Article
- Review
- Differential Proinflammatory Responses toJournal of fungi (Basel, Switzerland) · 2021Article
- Characterisation ofJournal of fungi (Basel, Switzerland) · 2021Article
- Fungal Infection and Inflammation in Cystic Fibrosis.Pathogens (Basel, Switzerland) · 2021Review
- Transcriptome Analysis of the Japanese Pine Sawyer Beetle,Journal of fungi (Basel, Switzerland) · 2021Article
- Dysregulation of Key Proteinases inReports of biochemistry & molecular biology · 2021Article
- EphA2-Dependent Internalization ofFrontiers in microbiology · 2020Article
- Phagolysosomal Survival Enables Non-lytic Hyphal Escape and Ramification Through Lung Epithelium DuringFrontiers in microbiology · 2020Article
- Interactions of an Emerging Fungal Pathogen Scedosporium aurantiacum with Human Lung Epithelial Cells.Scientific reports · 2019Article
- Phagocytosis ofFrontiers in cellular and infection microbiology · 2019Article
- Bioinformatic analysis of bacteria and host cell dual RNA-sequencing experiments.Briefings in bioinformatics · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundGiven the complex nature of the responses that can occur in host-pathogen interactions, dual transcriptomics offers a powerful method of elucidating these interactions during infection. The gene expression patterns of Aspergillus fumigatus conidia or host cells have been reported in a number of previous studies, but each focused on only one of the interacting organisms. In the present study, we profiled simultaneously the transcriptional response of both A. fumigatus and human airway epithelial cells (AECs). METHODOLOGY: 16HBE14o- transformed bronchial epithelial cells were incubated with A. fumigatus conidia at 37°C for 6 hours, followed by genome-wide transcriptome analysis using human and fungal microarrays. Differentially expressed gene lists were generated from the microarrays, from which biologically relevant themes were identified. Human and fungal candidate genes were selected for validation, using RT-qPCR, in both 16HBE14o- cells and primary AECs co-cultured with conidia. PRINCIPAL
findingsWe report that ontologies related to the innate immune response are activated by co-incubation with A. fumigatus condia, and interleukin-6 (IL-6) was confirmed to be up-regulated in primary AECs via RT-qPCR. Concomitantly, A. fumigatus was found to up-regulate fungal pathways involved in iron acquisition, vacuolar acidification, and formate dehydrogenase activity.
conclusionTo our knowledge, this is the first study to apply a dual organism transcriptomics approach to interactions of A. fumigatus conidia and human airway epithelial cells. The up-regulation of IL-6 by epithelia and simultaneous activation of several pathways by fungal conidia warrants further investigation as we seek to better understand this interaction in both health and disease. The cellular response of the airway epithelium to A. fumigatus is important to understand if we are to improve host-pathogen outcomes.
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