Project description:Global amphibian declines and extinction events are currently occurring at an unprecedented rate. While various factors are influencing these declines, one factor that is readily identifiable is disease. Specifically, the fungal pathogen Batrachochytrium dendrobatidis is thought to play a major role in amphibian declines in tropical and neotropical regions of the globe. While the effects of this chytrid fungus have been shown to be devastating, certain individuals and relict populations have shown resistance. This resistance has been attributed in part to the cutaneous microbiome. Many identified bacterial species that make up the microbiome have shown anti-B. dendrobatidis activity in vitro. One bacteria that is commonly associated as being a member of the amphibian microbiome across amphibian species and shows such anti-B. dendrobatidis activity is Serratia marcescens. Here, we look at transcriptomic shifts in gene expression of S. marcescens (high homology to strain WW4) in response to both live and heat-killed B. dendrobatidis.
Project description:Amphibian populations around the world are threatened by an emerging infectious pathogen, the chytrid fungus Batrachochytrium dendrobatidis (Bd). How can a fungal skin infection kill such a broad range of amphibian hosts? And why are certain species particularly susceptible to the impacts of Bd? Here we use a genomics approach to understand the genetic response of multiple susceptible frog species to Bd infection. We characterize the transcriptomes of two closely-related endangered frog species (Rana muscosa and Rana sierrae) and analyze whole genome expression profiles from frogs in controlled Bd-infection experiments. We integrate the Rana results with a comparable dataset from a more distantly-related susceptible species (Silurana tropicalis). We demonstrate that Bd-infected frogs show massive disruption of skin function and show no evidence of a robust immune response. The genetic response to infection is shared across the focal susceptible species, suggesting a common effect of Bd on susceptible frogs.
Project description:Chytridiomycosis is an emerging infectious disease of amphibians caused by the chytrid Batrachochytrium dendrobatidis (Bd). The disease has been associated with global amphibian declines and is driving the species in the wild to extinction. Using DNA microarray technology we have analysed transcriptional changes in Xenopus tropicalis during the course (7 and 42 days) of infection by Bd under warm (26oC) and cold (18oC) temperatures.
Project description:Amphibian populations around the world are threatened by an emerging infectious pathogen, the chytrid fungus Batrachochytrium dendrobatidis (Bd). How can a fungal skin infection kill such a broad range of amphibian hosts? And why are certain species particularly susceptible to the impacts of Bd? Here we use a genomics approach to understand the genetic response of multiple susceptible frog species to Bd infection. We characterize the transcriptomes of two closely-related endangered frog species (Rana muscosa and Rana sierrae) and analyze whole genome expression profiles from frogs in controlled Bd-infection experiments. We integrate the Rana results with a comparable dataset from a more distantly-related susceptible species (Silurana tropicalis). We demonstrate that Bd-infected frogs show massive disruption of skin function and show no evidence of a robust immune response. The genetic response to infection is shared across the focal susceptible species, suggesting a common effect of Bd on susceptible frogs. A total of five (12-plex) chips were analyzed from 60 samples comprising 2 conditions (control and infected), 3 tissues (skin, liver and spleen) and 2 timepoints (early and late). Three biological replicates were used for each condition and tissue at each time point. Twentyfour arrays were analyzed for skin samples, 24 for liver, and 12 for spleen. The same dye, Cy5, was used for all samples.
Project description:Type 2 immune responses are crucial for protection against helminth infections and for the maintenance of tissue homeostasis, yet the underlying mechanisms of immune activation remain incompletely understood. Here, we study the role of mast cells in type 2 immunity. While the number of lamina propria residing mast cells (termed LPMCs hereinafter) remained stable, intraepithelial mast cells (termed IEMCs hereinafter) markedly expanded during the course of type 2 responses. We uncovered a new type 2 response mechanism depending on the crosstalk between mast cells and epithelial cells, and defined the function of intraepithelial mast cells.
Project description:Mast cells are hematopoietic cells that reside preferentially in tissues exposed to internal and external environments. Mast cells sense immunological, inflammatory and environmental stimuli, and can be activated to release granules and generate inflammatory mediators. Mast cell-derived products confer protection against snake venoms and some parasite infections. Aberrant activation of mast cells is a major contributor to human pathology, including allergy, asthma and adverse drug reactions. Their strict tissue location has largely impeded the isolation of large numbers of primary mast cell for further analysis. To better understand the biology of mast cells, we analyzed the proteome of primary mouse mast cells by quantitative mass spectrometry