Aeromonas
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA260478 | ENA |
REPOSITORIES: ENA
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Project description:Aeromonas are ubiquitous inhabitants of both natural and anthropogenic aquatic ecosystems. Occasionally, Aeromonas also grows in drinking water distribution systems, which is highly undesired due to the pathogenicity of some members of this genus. The growth of Aeromonas in such highly oligotrophic environments is currently poorly understood. Possible nutrient sources are biopolymers. For example, chitin is the structural component of the exoskeleton of insects, some invertebrates and the cell walls of fungi which makes it one of the most abundant carbon and nitrogen sources in nature. In this study we demonstrate the ability of two Aeromonas strains, Aeromonas bestiarum and Aeromonas rivuli to efficiently grow on chitin. The secreted proteins confirm the presence of the functional hydrolytic enzymes that enable the efficient degradation and utilization of this abundant biopolymer. Further quantitative cellular proteomic study unravels the remarkable reorganization of the Aeromonas metabolism when switching to chitin as sole carbon and nitrogen source. This proves that Aeromonas is not only chitinolytic but also a chitinotrophic microorganism.
2024-12-12 | PXD047459 | Pride
Project description:Aeromonas caviae has been associated with human gastrointestinal disease. Strains of this species typically lack virulence factors (VFs) such as enterotoxins and hemolysins that are produced by other human pathogens of the Aeromonas genus. Microarray profiling of murine small intestinal extracts, 24 hours after oral infection with an A. caviae strain, provides evidence of a Th1 type immune response. A large number of gamma-interferon (γ-IFN) induced genes are up-regulated as well as several tumor necrosis factor-alpha (TNF-α) transcripts. A. caviae has always been considered an opportunistic pathogen because it lacks obvious virulence factors. This current effort suggests A. caviae colonizes murine intestinal tract and causes what has been described by others as a dysregulatory cytokine response leading to an irritable bowel-like syndrome. This response would explain why a number of diarrheal waterborne outbreaks have been attributed to A. caviae even though it lacks obvious enteropathogenic properties. Keywords: Aeromonas caviae, infection, disease mechanism, TH1 resposne
2007-01-20 | GSE6765 | GEO
Project description:Aims: To assess the virulence of multiple Aeromonas spp. using two models, a neonatal mouse assay and a mouse intestinal cell culture. Methods and Results: Transcriptional responses to both infection models were evaluated using microarrays. After artificial infection with a variety of Aeromonas spp., mRNA extracts from the two models were processed and hydridized to murine microarrays to determine host gene response. Definition of virulence was determined based on host mRNA production in murine neonatal intestinal tissue and mortality of infected animals. Infections of mouse intestinal cell cultures were then performed to determine whether this simpler model system's mRNA responses correlated to neonatal results and therefore be predictive of virulence of Aeromonas spp. Virulent aeromonads up-regulated transcripts in both models including multiple host defense gene products (chemokines, regulation of transcription and apoptosis, cell signaling). Avirulent species exhibited little or no host response in neonates. Mortality results correlated well with both bacterial dose and average fold change of up-regulated transcripts in the neonatal mice. Conclusions: Cell culture results were less discriminating but showed promise as potentially being able to be predictive of virulence. Jun oncogene up-regulation in murine cell culture is potentially predictive of Aeromonas virulence. Significance and Impact of the Study: Having the ability to determine virulence of waterborne pathogens quickly would potentially assist public health officials to rapidly assess exposure risks. Keywords: Aeromonas; Virulence; Gene expression; Host response
2006-10-21 | GSE6065 | GEO