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Multiple differences in pathogen-host cell interactions following a bacterial host shift.

ABSTRACT: Novel disease emergence is often associated with changes in pathogen traits that enable pathogen colonisation, persistence and transmission in the novel host environment. While understanding the mechanisms underlying disease emergence is likely to have critical implications for preventing infectious outbreaks, such knowledge is often based on studies of viral pathogens, despite the fact that bacterial pathogens may exhibit very different life histories. Here, we investigate the ability of epizootic outbreak strains of the bacterial pathogen, Mycoplasma gallisepticum, which jumped from poultry into North American house finches (Haemorhous mexicanus), to interact with model avian cells. We found that house finch epizootic outbreak strains of M. gallisepticum displayed a greater ability to adhere to, invade, persist within and exit from cultured chicken embryonic fibroblasts, than the reference virulent (R_low) and attenuated (R_high) poultry strains. Furthermore, unlike the poultry strains, the house finch epizootic outbreak strain HF_1994 displayed a striking lack of cytotoxicity, even exerting a cytoprotective effect on avian cells. Our results suggest that, at epizootic outbreak in house finches, M. gallisepticum was particularly adept at using the intra-cellular environment, which may have facilitated colonisation, dissemination and immune evasion within the novel finch host. Whether this high-invasion phenotype is similarly displayed in interactions with house finch cells, and whether it contributed to the success of the host shift, remains to be determined.

SUBMITTER: Dowling AJ

PROVIDER: S-EPMC7176683 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Multiple differences in pathogen-host cell interactions following a bacterial host shift.

Dowling Andrea J AJ Hill Geoffrey E GE Bonneaud Camille C

Scientific reports 20200422 1

Novel disease emergence is often associated with changes in pathogen traits that enable pathogen colonisation, persistence and transmission in the novel host environment. While understanding the mechanisms underlying disease emergence is likely to have critical implications for preventing infectious outbreaks, such knowledge is often based on studies of viral pathogens, despite the fact that bacterial pathogens may exhibit very different life histories. Here, we investigate the ability of epizoo ...[more]

PMID: 32322086

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Project description:The goal of this project is to understand the etiology and pathology of host-pathogen interaction using high-throughput cellular phenotyping. By combining the expertise in pathogen biology, informatics and stem cell biology across the institute, this project will use targeted genetic modification in mouse embryonic stem cells to identify functions of host genes in innate immunity. We will also explore the biology of mouse embryonic stem cells and their differentiation into immune competent cells. To this end we will generate homozygous and inducible knockout lines in mouse embryonic stem cells, which will be differentiated into immune competent cells, such as macrophages or dendritic cells. These will be subjected to a panel of immune challenge and stimulation assays to characterise the functions of the disrupted genes. To identify new functions for mammalian genes in innate immunity we will:\Generate a panel of homozygous inducible gene knockout mouse ES cell lines working from a list of ca. 80 candidate genes (MGP phenotyping and GWAS hits). \Scale up differentiation protocols for immune challenge and stimulation assays.\Benchmark in vitro differentiated ES cell models against primary immune cells from selected MGP mouse lines and eventually against human iPS cells.\Screen a panel of 30 genetically modified cell lines in immunological challenge and stimulation assays, defining phenotypes at the cellular level by high content imaging, biochemically by assaying cytokine production, and at the molecular level by transcriptome analysis.\Define novel gene functions in innate immunity through network analysis of gene expression data from all challenged cell lines.\In the longer term scale up the production and phenotyping of genetically modified cell lines (mouse or human as appropriate).This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

Dataset Information

Multiple differences in pathogen-host cell interactions following a bacterial host shift.

Publications

Multiple differences in pathogen-host cell interactions following a bacterial host shift.

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