ArticleInfection and immunity2006
ShiA abrogates the innate T-cell response to Shigella flexneri infection.
Article in Infection and immunity, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Locus of Adhesion and Autoaggregation (LAA) pathogenicity island genesMicrobiology spectrum · 2026Article
- Article
- Duplication and diversification of a unique chromosomal virulence island hosting the subtilase cytotoxin inMicrobial genomics · 2020Article
- Pathogenicity Factors of Genomic Islands in Intestinal and ExtraintestinalFrontiers in microbiology · 2020Review
- Investigating the Relatedness of Enteroinvasive Escherichia coli to Other E. coli and Shigella Isolates by Using Comparative Genomics.Infection and immunity · 2016Article
- Article
- Intracellular Shigella remodels its LPS to dampen the innate immune recognition and evade inflammasome activation.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Roles of H2 uptake hydrogenases in Shigella flexneri acid tolerance.Microbiology (Reading, England) · 2012Article
- Genomic characterization of enteroaggregative Escherichia coli from children in Mali.The Journal of infectious diseases · 2012Article
- Identification of Escherichia coli genes associated with urinary tract infections.Journal of clinical microbiology · 2012Article
- Uropathogenic Escherichia coli Suppresses the host inflammatory response via pathogenicity island genes sisA and sisB.Infection and immunity · 2009Article
- Article
- Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion.Clinical microbiology reviews · 2008Review
- Yeast functional genomic screens lead to identification of a role for a bacterial effector in innate immunity regulation.PLoS pathogens · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Shigella spp. are the causative agent of bacillary dysentery. Infection results in acute colonic injury due to the host inflammatory response. The mediators of the damage, infiltrating polymorphonuclear leukocytes (PMN), also resolve the infection. Shigella flexneri's virulence effectors are encoded on its large virulence plasmid and on pathogenicity islands in the chromosome. The SHI-2 pathogenicity island encodes the virulence factor ShiA, which down-regulates Shigella-induced inflammation. In the rabbit ileal loop model, infection with a shiA null strain (DeltashiA) induces a more severe inflammation than wild-type infection. Conversely, a Shigella strain that overexpresses ShiA (ShiA+) is less inflammatory than the wild-type strain. To determine the host responses modulated by ShiA, we performed infection studies using the mouse lung model, which recapitulates the phenotypes observed in the rabbit ileal loop model. Significantly, ShiA+ strain-infected mice cleared the bacteria and survived infection, while wild-type- and DeltashiA strain-infected mice could not clear the bacteria and ultimately died. Surprisingly, microarray analysis of infected lungs revealed the regulation of genes involved in innate T-cell responses to infection. Immunohistochemistry showed that wild-type- and DeltashiA strain-infected animals have greater numbers of PMN and T cells in their lungs over the course of infection than ShiA+ strain-infected animals. These results suggest that the T-cell innate response is suppressed by ShiA in Shigella infections.
Indexed as
Identifiers
What OpenQuestion holds
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.