ArticleInfection and immunity2013
Functional characterization of Burkholderia pseudomallei trimeric autotransporters.
Article in Infection and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Secretion systems shaping host-pathogen interactions in Burkholderia species.Applied microbiology and biotechnology · 2026Review
- Trigger Factor inJournal of bacteriology · 2026Article
- Review
- Review
- Comprehensive genome analysis of Burkholderia contaminans SK875, a quorum-sensing strain isolated from the swine.AMB Express · 2023Article
- Pathogenicity and virulence ofVirulence · 2022Review
- The C-terminal head domain of Burkholderia pseudomallei BpaC has a striking hydrophilic core with an extensive solvent network.Molecular microbiology · 2022Article
- An Evolutionary Arms Race BetweenFrontiers in microbiology · 2020Review
- Review
- Melioidosis.Nature reviews. Disease primers · 2018Review
- Use of Reverse Vaccinology in the Design and Construction of Nanoglycoconjugate Vaccines against Burkholderia pseudomallei.Clinical and vaccine immunology : CVI · 2017Article
- Antibodies againstInfection and immunity · 2017Article
- An avirulent Burkholderia pseudomallei ∆purM strain with atypical type B LPS: expansion of the toolkit for biosafe studies of melioidosis.BMC microbiology · 2017Article
- Characterization of the murine macrophage response to infection with virulent and avirulent Burkholderia species.BMC microbiology · 2015Article
- Article
- The Autotransporter BpaB Contributes to the Virulence of Burkholderia mallei in an Aerosol Model of Infection.PloS one · 2015Article
- Melioidosis: molecular aspects of pathogenesis.Expert review of anti-infective therapy · 2014Review
- Characterization of an autotransporter adhesin protein shared by Burkholderia mallei and Burkholderia pseudomallei.BMC microbiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Burkholderia pseudomallei is a tier 1 select agent and the causative agent of melioidosis, a severe and often fatal disease with symptoms ranging from acute pneumonia and septic shock to a chronic infection characterized by abscess formation in the lungs, liver, and spleen. Autotransporters (ATs) are exoproteins belonging to the type V secretion system family, with many playing roles in pathogenesis. The genome of B. pseudomallei strain 1026b encodes nine putative trimeric AT proteins, of which only four have been described. Using a bioinformatic approach, we annotated putative domains within each trimeric AT protein, excluding the well-studied BimA protein, and found short repeated sequences unique to Burkholderia species, as well as an unexpectedly large proportion of ATs with extended signal peptide regions (ESPRs). To characterize the role of trimeric ATs in pathogenesis, we constructed disruption or deletion mutations in each of eight AT-encoding genes and evaluated the resulting strains for adherence to, invasion of, and plaque formation in A549 cells. The majority of the ATs (and/or the proteins encoded downstream) contributed to adherence to and efficient invasion of A549 cells. Using a BALB/c mouse model of infection, we determined the contributions of each AT to bacterial burdens in the lungs, liver, and spleen. At 48 h postinoculation, only one strain, Bp340::pDbpaC, demonstrated a defect in dissemination and/or survival in the liver, indicating that BpaC is required for wild-type virulence in this model.
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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.