Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1200765 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31784100_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR31784200_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR31784101_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR31784201_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR31784102_subreads.fastq.gz | Fastqsanger.gz |
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Project description:The role of domestic and peridomestic animals in vector-borne diseases is very important as they share a common environment with people having the potential to extend the network of pathogen transmission to humans. The most significant vector-borne infectious diseases that are shared by man, domestic and peridomestic animals are leishmaniosis, borreliosis, bartonellosis, ehrlichiosis, rickettsiosis and anaplasmosis with fleas acting as main vectors in the transmission of some of these diseases. Flea-borne diseases which are relevant in Europe include plague (caused by Yersinia pestis), murine typhus (caused by Rickettsia typhi), flea-borne spotted fever (Rickettsia felis), and cat scratch disease (Bartonella henselae). In the present study, mNGS was applied to detect and understand the composition of the microbial communities of five different species of fleas (Archaeopsylla erinacei, Ctenocephalides felis, Spilopsyllus cuniculi, Pulex irritans and Ctenocephalides canis) collected on dogs, cats and hedgehogs from Andalusia (Spain) to know the prevalence of pathogenic bacteria among synanthropic fleas. Based on our results, we could conclude that Pulicidae family encompassed those flea species with a close contact with humans and therefore more involved in the potential transmission of infectious diseases. The higher relative abundance of the Phylum Pseudomanadota was mainly due to the presence of the endosymbiont Wolbachia, as well as to notice a high relative abundance of both genera Rickettsia and Bartonella in all flea species. For the first time, we detected Babesia sp. in all species tested, especially with higher abundance in S. cuniculi collected from cats emphasizing the need for further investigation into its potential implications as vectors. Our results also demonstrate that the microbiota composition of fleas is largely influenced by the host they parasitize. Lastly, statistical analyses of microbiota allowed for the ecological separation of flea species, with individuals from these five species clustering distinctly each other.
2025-09-24 | GSE284667 | GEO
Project description:Yersinia pestis, the etiologic agent of plague, emerged as a flea-borne pathogen only within the last 6,000 years. Just five simple genetic changes in the Yersinia pseudotuberculosis progenitor, which served to eliminate toxicity to fleas and to enhance survival and biofilm formation in the flea digestive tract, were key to the transition to the arthropod-borne transmission route. To gain a deeper understanding of the genetic basis for the development of a transmissible biofilm infection in the flea foregut, we evaluated additional gene differences and performed in vivo transcriptional profiling of Y. pestis, Y. pseudotuberculosis wild-type (unable to form biofilm in the flea foregut), and a Y. pseudotuberculosis mutant strain (able to produce foregut-blocking biofilm in fleas) recovered from fleas 1 day and 14 days after an infectious bloodmeal. Surprisingly, the Y. pseudotuberculosis mutations that increased c-di-GMP levels and enabled biofilm development in the flea did not change expression levels of the hms genes responsible for the synthesis and export of the extracellular polysaccharide matrix required for mature biofilm formation. The Y. pseudotuberculosis mutant uniquely expressed much higher levels of one of the Yersinia Type VI secretion systems (T6SS-4) in the flea, and this locus was required for flea blockage by Y. pseudotuberculosis, but not by Y. pestis. Significant differences between the two species in expression of several metabolism genes, the Psa fimbrial genes, quorum sensing related genes, transcriptional regulators, and stress response genes were evident during flea infection. The results provide insights into how Y. pestis has adapted to life in its flea vector and point to evolutionary changes in the regulation of biofilm development pathways in these two closely related species
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Project description:Yersinia pestis, the agent of plague, is transmitted to mammals by infected fleas. Y. pestis exhibits a distinct life stage in the flea, where it grows in the form of a cohesive biofilm that promotes transmission. After transmission, the temperature shift to 37°C induces many known virulence factors of Y. pestis that confer resistance to innate immunity. These factors are not produced in the low-temperature environment of the flea, however, suggesting that Y. pestis is vulnerable to the initial encounter with innate immune cells at the flea bite site. In this study, we used whole-genome microarrays to compare the Y. pestis in vivo transcriptome in infective fleas to in vitro transcriptomes in temperature-matched biofilm and planktonic cultures, and to the previously characterized in vivo gene expression profile in the rat bubo. In addition to genes involved in metabolic adaptation to the flea gut and biofilm formation, several genes with known or predicted roles in resistance to innate immunity and pathogenicity in the mammal were upregulated in the flea. Y. pestis from infected fleas were more resistant to phagocytosis than in vitro-grown bacteria, which was largely attributable to a cluster of insecticidal-like toxin genes that were highly expressed only in the flea. Our results indicate that cycling through the flea vector preadapts Y. pestis to face the mammalian innate immune response that it encounters immediately after transmission. Midlog phase vs. stationary phase vs. flowcell biofilm vs. flea biofilm.
2010-04-06 | E-GEOD-16493 | biostudies-arrayexpress
Project description:Yersinia pestis, the agent of plague, is transmitted to mammals by infected fleas. Y. pestis exhibits a distinct life stage in the flea, where it grows in the form of a cohesive biofilm that promotes transmission. After transmission, the temperature shift to 37°C induces many known virulence factors of Y. pestis that confer resistance to innate immunity. These factors are not produced in the low-temperature environment of the flea, however, suggesting that Y. pestis is vulnerable to the initial encounter with innate immune cells at the flea bite site. In this study, we used whole-genome microarrays to compare the Y. pestis in vivo transcriptome in infective fleas to in vitro transcriptomes in temperature-matched biofilm and planktonic cultures, and to the previously characterized in vivo gene expression profile in the rat bubo. In addition to genes involved in metabolic adaptation to the flea gut and biofilm formation, several genes with known or predicted roles in resistance to innate immunity and pathogenicity in the mammal were upregulated in the flea. Y. pestis from infected fleas were more resistant to phagocytosis than in vitro-grown bacteria, which was largely attributable to a cluster of insecticidal-like toxin genes that were highly expressed only in the flea. Our results indicate that cycling through the flea vector preadapts Y. pestis to face the mammalian innate immune response that it encounters immediately after transmission.
2010-04-06 | GSE16493 | GEO
Project description:The Yersinia pestis PhoPQ gene regulatory system is induced during infection of the flea digestive tract and is required to produce adherent biofilm in the foregut, which greatly enhances bacterial transmission during a flea bite. To understand the in vivo context of PhoPQ induction and to determine PhoP-regulated targets in the flea, we undertook whole genome comparative transcriptional profiling of Y. pestis wild-type and ΔphoP strains isolated from infected fleas and from temperature-matched in vitro planktonic and flowcell biofilm cultures. In the absence of PhoP regulation, the gene expression program indicated that the bacteria experience diverse physiological stresses and are in a metabolically less active state. Multiple stress response genes, including several toxin-antitoxin loci and YhcN family genes responsible for increased acid tolerance, were upregulated in the phoP mutant during flea infection. The data imply that PhoPQ is induced by low pH in the flea gut, and that PhoP modulates physiologic adaptation to acid and other stresses encountered during infection of the flea. This adaptive response, together with PhoP-dependent modification of the bacterial outer surface that includes repression of pH 6 antigen fimbriae, supports stable biofilm development in the flea foregut.
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Project description:The purpose of this study was the identification of RNAs contained in the urinary exosome (UExo) from dogs and cats. The quality of total RNA in isolated urinary exosome (UExo)-derived total RNAs obtained from the column-based method (urine 1 mL) was checked by using a Bioanalyzer, and samples from normal renal function (NR) group and kidney disease (KD) group were pooled as one sample for each group. We collected NR dogs (n = 37), KD dogs (n = 47), NR cats (n=43), and KD cats (n = 45). For the next generation sequencing, libraries were prepared according to the manufacturer’s protocols and sequenced using 50-base reads acquired by using a HiSeq 2000 platform. The December 2011 (GRCm38/mm10) mouse (Mus musculus) genome data were used as reference. As a result, we could identify the miRNA from these samples.
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