scholarly journals Burkholderia cenocepacia Type VI Secretion System Mediates Escape of Type II Secreted Proteins into the Cytoplasm of Infected Macrophages

PLoS ONE â—½  
2012 â—½  
Vol 7 (7) â—½  
pp. e41726 â—½  
Author(s):  
Roberto Rosales-Reyes â—½  
Daniel F. Aubert â—½  
Jennifer S. Tolman â—½  
Amal O. Amer â—½  
Miguel A. Valvano
Keyword(s):  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Secreted Proteins â—½  
Type Ii â—½  
Type Vi Secretion System â—½  
Type Vi Secretion

scholarly journals Burkholderia cenocepacia utilizes a type VI secretion system for bacterial competition

MicrobiologyOpen â—½  
10.1002/mbo3.774 â—½  
2019 â—½  
Vol 8 (7) â—½  
Author(s):  
Helena L. Spiewak â—½  
Sravanthi Shastri â—½  
Lili Zhang â—½  
Stephan Schwager â—½  
Leo Eberl â—½  
...  
Keyword(s):  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Type Vi Secretion System â—½  
Bacterial Competition â—½  
Type Vi Secretion

scholarly journals Host Adaptation Predisposes Pseudomonas aeruginosa to Type VI Secretion System-Mediated Predation by the Burkholderia cepacia Complex

2020 â—½  
Author(s):  
Andrew I Perault â—½  
Courtney E Chandler â—½  
David A Rasko â—½  
Robert K Ernst â—½  
Matthew C Wolfgang â—½  
...  
Keyword(s):  
Pseudomonas Aeruginosa â—½  
Burkholderia Cepacia â—½  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Burkholderia Cepacia Complex â—½  
Dependent Manner â—½  
Type Vi Secretion System â—½  
Secretion Systems â—½  
Type Vi Secretion

SUMMARYPseudomonas aeruginosa (Pa) and Burkholderia cepacia complex (Bcc) species are opportunistic lung pathogens of individuals with cystic fibrosis (CF). While Pa can initiate long-term infections in younger CF patients, Bcc infections only arise in teenagers and adults. Both Pa and Bcc use type VI secretion systems (T6SS) to mediate interbacterial competition. Here, we show that Pa isolates from teenage/adult CF patients, but not those from young CF patients, are outcompeted by the epidemic Bcc isolate Burkholderia cenocepacia strain AU1054 (BcAU1054) in a T6SS-dependent manner. The genomes of susceptible Pa isolates harbor T6SS-abrogating mutations, the repair of which, in some cases, rendered the isolates resistant. Moreover, seven of eight Bcc strains outcompeted Pa strains isolated from the same patients. Our findings suggest that certain mutations that arise as Pa adapts to the CF lung abrogate T6SS activity, making Pa and its human host susceptible to potentially fatal Bcc superinfection.

scholarly journals The Burkholderia cenocepacia type VI secretion system effector TecA is a virulence factor during lung infection

2021 â—½  
Author(s):  
Nicole A. Loeven â—½  
Andrew I. Perault â—½  
Peggy A. Cotter â—½  
Craig A. Hodges â—½  
Joseph D. Schwartzman â—½  
...  
Keyword(s):  
Weight Loss â—½  
Clinical Isolate â—½  
Virulence Factor â—½  
Lung Infection â—½  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Burkholderia Cepacia Complex â—½  
Type Vi Secretion System â—½  
Type Vi Secretion â—½  
Lung Infections

Burkholderia cenocepacia (Bc) is a member of the Burkholderia cepacia complex (Bcc), a group of bacteria with members responsible for causing lung infections in cystic fibrosis (CF) patients. The most severe outcome of Bcc infection in CF patients is cepacia syndrome, a disease characterized by necrotizing pneumonia with bacteremia and sepsis. Bc is strongly associated with cepacia syndrome making it one of the most virulent members of the Bcc. Mechanisms underlying the pathogenesis of Bc in lung infections and cepacia syndrome remain to be uncovered. Bc is primarily an intracellular pathogen, and encodes the type VI secretion system (T6SS) anti-host effector TecA, which is translocated into host cells. TecA is a deamidase that inactivates multiple Rho GTPases, including RhoA. Inactivation of RhoA by TecA triggers assembly of the pyrin inflammasome, leading to secretion of proinflammatory cytokines such as IL-1β from macrophages. Previous work with the Bc clinical isolate J2315 showed that TecA increases immunopathology during acute lung infection in C57BL/6 mice and suggested that this effector acts as a virulence factor by triggering assembly of the pyrin inflammasome. Here, we extend these results using a second Bc clinical isolate, AU1054, to demonstrate that TecA exacerbates weight loss and lethality during lung infection in C57BL/6 mice and CF mice. Unexpectedly, pyrin was dispensable for TecA virulence activity in both mouse infection models. Our findings establish that TecA is a Bc virulence factor that exacerbates lung inflammation, weight loss, and lethality in a mouse lung infection model.

scholarly journals Quantification of type VI secretion system activity in macrophages infected with Burkholderia cenocepacia

Microbiology â—½  
2015 â—½  
Vol 161 (11) â—½  
pp. 2161-2173 â—½  
Author(s):  
Daniel F. Aubert â—½  
Miguel A. Valvano â—½  
Sherry Hu
Keyword(s):  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Type Vi Secretion System â—½  
System Activity â—½  
Type Vi Secretion

scholarly journals TssA from Burkholderia cenocepacia: expression, purification, crystallization and crystallographic analysis

2018 â—½  
Vol 74 (9) â—½  
pp. 536-542 â—½  
Author(s):  
Hayley J. Owen â—½  
Ruyue Sun â—½  
Asma Ahmad â—½  
Svetlana E. Sedelnikova â—½  
Patrick J. Baker â—½  
...  
Keyword(s):  
Phylogenetic Analysis â—½  
Structure Determination â—½  
Crystallographic Analysis â—½  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Type Vi Secretion System â—½  
Core Component â—½  
The Third â—½  
Terminal Domain â—½  
Type Vi Secretion

TssA is a core component of the type VI secretion system, and phylogenetic analysis of TssA subunits from different species has suggested that these proteins fall into three distinct clades. Whilst representatives of two clades, TssA1 and TssA2, have been the subjects of investigation, no members of the third clade (TssA3) have been studied. Constructs of TssA from Burkholderia cenocepacia, a representative of clade 3, were expressed, purified and subjected to crystallization trials. Data were collected from crystals of constructs of the N-terminal and C-terminal domains. Analysis of the data from the crystals of these constructs and preliminary structure determination indicates that the C-terminal domain forms an assembly of 32 subunits in D 16 symmetry, whereas the N-terminal domain is not involved in subunit assocation.

scholarly journals The Burkholderia cenocepacia Type VI Secretion System Effector TecA Is a Virulence Factor in Mouse Models of Lung Infection

mBio â—½  
2021 â—½  
Author(s):  
Nicole A. Loeven â—½  
Andrew I. Perault â—½  
Peggy A. Cotter â—½  
Craig A. Hodges â—½  
Joseph D. Schwartzman â—½  
...  
Keyword(s):  
Animal Model â—½  
Mouse Models â—½  
Close Association â—½  
Lung Infection â—½  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Type Vi Secretion System â—½  
Content Type â—½  
Type Vi Secretion â—½  
Lung Infections

B. cenocepacia is often considered the most virulent species in the Bcc because of its close association with cepacia syndrome in addition to its capacity to cause chronic lung infections in CF patients (1). Prior to the current study, virulence factors of B. cenocepacia important for causing lethal disease had not been identified in a CF animal model of lung infection.

The Type VI secretion system of Burkholderia cenocepacia affects multiple Rho family GTPases disrupting the actin cytoskeleton and the assembly of NADPH oxidase complex in macrophages

2011 â—½  
Vol 14 (2) â—½  
pp. 255-273 â—½  
Author(s):  
Roberto Rosales-Reyes â—½  
Alexander M. Skeldon â—½  
Daniel F. Aubert â—½  
Miguel A. Valvano
Keyword(s):  
Nadph Oxidase â—½  
Actin Cytoskeleton â—½  
Secretion System â—½  
Burkholderia Cenocepacia â—½  
Type Vi Secretion System â—½  
Type Vi Secretion â—½  
Rho Family Gtpases â—½  
Nadph Oxidase Complex â—½  
Rho Family

scholarly journals Conversion of a defensive toxin-antitoxin system into an offensive T6SS effector in Burkholderia

10.1101/835710 â—½  
2019 â—½  
Author(s):  
Sunil Kumar Yadav â—½  
Ankita Magotra â—½  
Aiswarya Krishnan â—½  
Srayan Ghosh â—½  
Rahul Kumar â—½  
...  
Keyword(s):  
Genome Analysis â—½  
Endophytic Bacteria â—½  
Secretion System â—½  
Genetic Change â—½  
Functional Similarity â—½  
Type Ii â—½  
Type Vi Secretion System â—½  
Defensive Function â—½  
Type Vi Secretion â—½  
Burkholderia Gladioli

Bacteria use various kinds of toxins to either inhibit the growth of co-habiting bacteria or when needed control their own growth. Here we report that Burkholderia and certain other bacteria have altered the potential defensive function of Tox-REase-5 domain containing toxins into offensive function. The Burkholderia gladioli strain NGJ1 encodes such toxins as type VI secretion system (T6SS) effectors (Tse) and potentially deploys them to kill co-habiting rice endophytic bacteria. Notably, the immunity (Tsi) proteins associated with Tse effectors demonstrate functional similarity with the antitoxin of type II toxin-antitoxin (TA) system. Genome analysis of diverse bacteria revealed that various Tse orthologs are either encoded as TA or T6SS effectors. In addition, potential evolutionary events associated with conversion of TA into T6SS effectors have been delineated. Our results indicate that the transposition of IS3 elements has led to the operonic fusion of certain T6SS related genes with TA genes resulting in their conversion into T6SS effectors. Such a genetic change has enabled bacteria to utilize novel toxins to precisely target co-habiting bacteria.

scholarly journals A Novel Sensor Kinase-Response Regulator Hybrid Controls Biofilm Formation and Type VI Secretion System Activity in Burkholderia cenocepacia

2008 â—½  
Vol 76 (5) â—½  
pp. 1979-1991 â—½  
Author(s):  
Daniel F. Aubert â—½  
Ronald S. Flannagan â—½  
Miguel A. Valvano
Keyword(s):  
Response Regulator â—½  
Secretion System â—½  
Lung Epithelial Cells â—½  
Burkholderia Cenocepacia â—½  
Infection Model â—½  
Sensor Kinase â—½  
Type Vi Secretion System â—½  
Macrophage Infection â—½  
Type Vi Secretion

ABSTRACT Burkholderia cenocepacia is an important opportunistic pathogen causing serious chronic infections in patients with cystic fibrosis (CF). Adaptation of B. cenocepacia to the CF airways may play an important role in the persistence of the infection. We have identified a sensor kinase-response regulator (BCAM0379) named AtsR in B. cenocepacia K56-2 that shares 19% amino acid identity with RetS from Pseudomonas aeruginosa. atsR inactivation led to increased biofilm production and a hyperadherent phenotype in both abiotic surfaces and lung epithelial cells. Also, the atsR mutant overexpressed and hypersecreted an Hcp-like protein known to be specifically secreted by the type VI secretion system (T6SS) in other gram-negative bacteria. Amoeba plaque assays demonstrated that the atsR mutant was more resistant to Dictyostelium predation than the wild-type strain and that this phenomenon was T6SS dependent. Macrophage infection assays also demonstrated that the atsR mutant induces the formation of actin-mediated protrusions from macrophages that require a functional Hcp-like protein, suggesting that the T6SS is involved in actin rearrangements. Three B. cenocepacia transposon mutants that were found in a previous study to be impaired for survival in chronic lung infection model were mapped to the T6SS gene cluster, indicating that the T6SS is required for infection in vivo. Together, our data show that AtsR is involved in the regulation of genes required for virulence in B. cenocepacia K56-2, including genes encoding a T6SS.

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