Evolutionary study on O96:H19 EIEC
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB35723 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3721842.fastq.gz | Fastqsanger.gz | |||
| ERR3721843.fastq.gz | Fastqsanger.gz | |||
| ERR3721844.fastq.gz | Fastqsanger.gz |
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Project description:The invasive bacteria recognition by host cells through autophagy is a key factor for determining bacterial infection. Enteroinvasive Escherichia coli (EIEC) express a protein IcsB, which in Shigella, is known for inactivating the bacterial degradation process. Once EIEC showed less expression of icsB when compared to S. flexneri, we proposed to investigate the autophagy caused by EIEC infection. Our results showed that IcsB protein is an important virulence factor in EIEC because it causes a camouflage of the bacteria in the eukaryotic cell. When there is low or none expression of the protein, the cell recognition of the invasive bacteria is high, decreasing the bacteria dissemination. This found confirms the importance of the gene transcription and the sequence, since the strain E. coli SM124/13, complemented with icsB from Shigella, showed higher dissemination efficiency inside of the host cell. Additionally, our results revealed that eukaryotic cell infected by EIEC or Shigella flexneri showed distinguish responses. In EIEC infection, the autophagy was activated in human cells, but not in a conventional mode. Our hypothesis is that EIEC is recognized by autophagy, being an important cell process for bacterial recognition.
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Project description:The invasive bacteria recognition by host cells through autophagy is a key factor for determining bacterial infection. Enteroinvasive Escherichia coli (EIEC) express a protein IcsB, which in Shigella, is known for inactivating the bacterial degradation process. Once EIEC showed less expression of icsB when compared to S. flexneri, we proposed to investigate the autophagy caused by EIEC infection. Our results showed that IcsB protein is an important virulence factor in EIEC because it causes a camouflage of the bacteria in the eukaryotic cell. When there is low or none expression of the protein, the cell recognition of the invasive bacteria is high, decreasing the bacteria dissemination. This found confirms the importance of the gene transcription and the sequence, since the strain E. coli SM124/13, complemented with icsB from Shigella, showed higher dissemination efficiency inside of the host cell. Additionally, our results revealed that eukaryotic cell infected by EIEC or Shigella flexneri showed distinguish responses. In EIEC infection, the autophagy was activated in human cells, but not in a conventional mode. Our hypothesis is that EIEC is recognized by autophagy, being an important cell process for bacterial recognition.
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Project description:The invasive bacteria recognition by host cells through autophagy is a key factor for determining bacterial infection. Enteroinvasive Escherichia coli (EIEC) express a protein IcsB, which in Shigella, is known for inactivating the bacterial degradation process. Once EIEC showed less expression of icsB when compared to S. flexneri, we proposed to investigate the autophagy caused by EIEC infection. Our results showed that IcsB protein is an important virulence factor in EIEC because it causes a camouflage of the bacteria in the eukaryotic cell. When there is low or none expression of the protein, the cell recognition of the invasive bacteria is high, decreasing the bacteria dissemination. This found confirms the importance of the gene transcription and the sequence, since the strain E. coli SM124/13, complemented with icsB from Shigella, showed higher dissemination efficiency inside of the host cell. Additionally, our results revealed that eukaryotic cell infected by EIEC or Shigella flexneri showed distinguish responses. In EIEC infection, the autophagy was activated in human cells, but not in a conventional mode. Our hypothesis is that EIEC is recognized by autophagy, being an important cell process for bacterial recognition.
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