Host Adaptation Predisposes<i>Pseudomonas aeruginosa</i>to Type VI Secretion System-Mediated Predation by the<i>Burkholderia cepacia</i>Complex

Perault, Andrew I.; Chandler, Courtney E.; Rasko, David A.; Ernst, Robert K.; Wolfgang, Matthew C.; Cotter, Peggy A.

doi:10.1101/2020.04.10.036012

Cited by 10 publications

(14 citation statements)

References 96 publications

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“…Hence, some commensals and/or pathogens protect themselves from intoxication through the utilization of a superior T6SS, while loss of their T6SS activity makes them vulnerable to assaults from competitors. This finding is in line with a recent study by Perault and colleagues whereby the authors showed that P. aeruginosa strains isolated from young cystic fibrosis patients are protected from Burkholderia cepacia complex (Bcc) pathogens in a T6SS-dependent manner 45 . However, during adaption to the host, P. aeruginosa strains often acquire T6SS-abrogating mutations, which render them susceptible to T6SS assaults from Bcc strains 45 .…”

Section: Resultssupporting

confidence: 91%

Human commensal gut Proteobacteria withstand type VI secretion attacks through immunity protein-independent mechanisms

et al. 2021

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While the major virulence factors for Vibrio cholerae, the cause of the devastating diarrheal disease cholera, have been extensively studied, the initial intestinal colonization of the bacterium is not well understood because non-human adult animals are refractory to its colonization. Recent studies suggest the involvement of an interbacterial killing device known as the type VI secretion system (T6SS). Here, we tested the T6SS-dependent interaction of V. cholerae with a selection of human gut commensal isolates. We show that the pathogen efficiently depleted representative genera of the Proteobacteria in vitro, while members of the Enterobacter cloacae complex and several Klebsiella species remained unaffected. We demonstrate that this resistance against T6SS assaults was mediated by the production of superior T6SS machinery or a barrier exerted by group I capsules. Collectively, our data provide new insights into immunity protein-independent T6SS resistance employed by the human microbiota and colonization resistance in general.

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Section: Resultssupporting

confidence: 91%

Human commensal gut Proteobacteria withstand type VI secretion attacks through immunity protein-independent mechanisms

et al. 2021

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“…However, bacterial interactions are diverse, and the involvement of specific mechanisms largely depend on cell-to-cell distance and the environment (Figure 6C). In close cell-to-cell interactions, injection structures, e.g., the T6SS (Lin et al, 2019;Lopez et al, 2020;Molina-Santiago et al, 2019;Perault et al, 2020), ensure the efficient delivery of the inhibitory compounds, while in longdistance interactions, diffusible molecules are more important (Deveau et al, 2016;Tyc et al, 2017). Inhibitory molecules are not always produced or concentrated at lethal levels, and alternative modes of action that induce changes in gene expression patterns or in modulation of the behavior of the competitor have emerged (Andersson and Hughes, 2014;Molina-Santiago et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Chemical interplay and complementary adaptative strategies toggle bacterial antagonism and co-existence

Molina‐Santiago¹,

Vela‐Corcía²,

Petras³

et al. 2021

Cell Reports

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“…Moreover, attenuation of T6SS in P. aeruginosa may give opportunities to other bacterial pathogens to outcompete itself and making host cells susceptible to subsequent infections. A recent research showed that P. aeruginosa abrogating its T6SS could be outcompeted by coinfecting B.cenocepaica in CF patients in an age-and T6SS-dependent manner and predisposing host to superinfection of B.cenocepaica [44].…”

Section: Discussionmentioning

confidence: 99%

NosocomialPseudomonas aeruginosaregulates alginate biosynthesis and Type VI secretion system during adaptive and convergent evolution for coinfection in critically ill COVID-19 patients

Jian

Cai

Duan

et al. 2021

Preprint

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COVID-19 pandemic has caused millions of death globally and caused huge impact on the health of infected patients. Shift in the lung microbial ecology upon such viral infection often worsens the disease and increases host susceptibility to secondary infections. Recent studies have indicated that bacterial coinfection is an unignorable factor contributing to the aggravation of COVID-19 and posing great challenge to clinical treatments. However, there is still a lack of in-depth investigation on the coinfecting bacteria in COVID-19 patients for better treatment of bacterial coinfection. With the knowledge that Pseudomonas aeruginosa is one of the top coinfecting pathogens, we analyzed the adaptation and convergent evolution of nosocomial Pseudomonas aeruginosa isolated from two critical COVID-19 patients in this study. We sequenced and compared the genomes and transcriptomes of Pseudomonas aeruginosa isolates longitudinally and parallelly for its evolutionary traits. Pseudomonas aeruginosa overexpressed alginate and attenuated Type VI secretion system (T6SS) during coinfection for excessive biofilm formation and suppressed virulence. Results of bacterial competition assay and macrophage cytotoxicity test indicated that Pseudomonas aeruginosa reduced its virulence towards both prokaryotic competitors and eukaryotic host through inhibiting its T6SS during evolution. Pseudomonas aeruginosa T6SS is thus one of the reasons for its advantage to cause coinfection in COVID-19 patients while the attenuation of T6SS could cause a shift in the microecological composition in the lung. Our study will contribute to the development of therapeutic measures and the discovery of novel drug target to eliminate Pseudomonas aeruginosa coinfection in COVID-19 patient.

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Host Adaptation PredisposesPseudomonas aeruginosato Type VI Secretion System-Mediated Predation by theBurkholderia cepaciaComplex

Cited by 10 publications

References 96 publications

Human commensal gut Proteobacteria withstand type VI secretion attacks through immunity protein-independent mechanisms

Human commensal gut Proteobacteria withstand type VI secretion attacks through immunity protein-independent mechanisms

Chemical interplay and complementary adaptative strategies toggle bacterial antagonism and co-existence

NosocomialPseudomonas aeruginosaregulates alginate biosynthesis and Type VI secretion system during adaptive and convergent evolution for coinfection in critically ill COVID-19 patients

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