ArticleVirulence2018
A type 6 secretion system (T6SS) encoded gene within Salmonella enterica serovar Enteritidis contributes to virulence.
Article in Virulence, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
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- Comparative genomic analysis provides new insights into non-typhoidal Salmonella population structure in Peru.Scientific reports · 2024Article
- Article
- TheFrontiers in cellular and infection microbiology · 2022Article
- Article
- Confirmed and Potential Roles of Bacterial T6SSs in the Intestinal Ecosystem.Frontiers in microbiology · 2019Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacteria interact with their host through protein secretion systems and surface structures. Pathogenic bacteria encode protein secretion systems that promote the invasion of the host's tissue, the evasion of the host's immune response, the thwarting microbial competitors, and ultimately survival within the host. For motile bacteria, the presence of extracellular flagella provides the host with a structural motif used for activation of the immune system. Within this issue of Virulence, the article "Identification of a novel gene in ROD9 island of Salmonella Enteritidis involved in the alteration of virulence-associated protein expression" describes the contribution of a gene, SEN1005, toward host-pathogen interaction. The authors demonstrate the contribution of SEN1005 to cell culture bioassays and infection in a mouse model of colitis. In each tested scenario, deletion of SEN1005 results in a phenotypic defect that was complemented by providing the SEN1005 gene in trans. SEN1005 contributes to the expression of known virulence factors within SPI-1, flagellar and chemotaxis genes, and heat shock/chaperone genes. Although much work is needed to fully elucidate the function of SEN1005, this work contributes toward our understanding of the genetic factors used by Salmonella to cause foodborne illnesses.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.