Transcriptional profiling of Pseudomonas aeruginosa and Staphylococcus aureus during in vitro co-culture

Tognon, Mikaël; Köhler, Thilo; Lüscher, Alexandre; Delden, Christian van

doi:10.1186/s12864-018-5398-y

Cited by 72 publications

(82 citation statements)

References 57 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The down-regulation of expression observed may certainly lead to a defect in ATP production. Conversely, we observed the increased expression of several dehydrogenase enzymes, suggesting a shift from aerobic respiration to lactic acid fermentation to feed the Krebs cycle, as shown previously in laboratory strains 33,34 . Certain dehydrogenases, such as adhE and gluD genes, are also implicated in oxidative stress responses 35 .…”

Section: Discussionsupporting

confidence: 88%

Coexistence withPseudomonas aeruginosaaltersStaphylococcus aureustranscriptome, antibiotic resistance and internalization into epithelial cells

Briaud

Camus

Bastien

et al. 2019

Preprint

View full text Add to dashboard Cite

15Cystic fibrosis (CF) is the most common life-threatening genetic disease among Caucasians. CF 16 patients suffer from chronic lung infections due to the presence of thick mucus, caused by cftr 17 gene dysfunction. The two most commonly found bacteria in the mucus of CF patients are 18Staphylococcus aureus and Pseudomonas aeruginosa. It is well known that early-infecting P. 19 aeruginosa strains produce anti-staphylococcal compounds and inhibit S. aureus growth. More 20 recently, it has been shown that late-infecting P. aeruginosa strains develop commensal-21 like/coexistence interaction with S. aureus. The aim of this study was to decipher the impact of P. 22While P. aeruginosa is recognized as the leading cause of lung function decline, the significance 49 of S. aureus in the course of CF disease is still being debated. It has been shown that one of the 50 risk factors for initial P. aeruginosa airway infection includes S. aureus pre-colonization [8][9][10] . 51However, the impact of coinfection by the two pathogens on the evolution of the disease remains 52 unclear 11-13 . 53 S. aureus and P. aeruginosa have been identified in the same lobe of CF lungs 14,15 , suggesting 54 that both pathogens are present in the same niche and can in fact interact in vivo. Interactions 55 4 have been widely studied and it is commonly admitted that P. aeruginosa outcompetes S. aureus. 56 Different mechanisms have been described 16 : for example, P. aeruginosa secreted products can 57 inhibit the growth or lyse S. aureus as well as induce epithelial cells to kill S. aureus and other 58Gram-positive bacteria 8,17,18 . 59 However, these interactions can evolve during chronic colonization. Indeed, P. aeruginosa strains 60 isolated from early infection outcompete S. aureus, as previously described, while strains isolated 61 from chronic infection are less aggressive and can be co-cultivated with S. aureus 19,20 . 62 Furthermore, P. aeruginosa isolates from mono-infected patients are more competitive towards S. 63 aureus than isolates from coinfected patients 21 . 64 In contrast to antagonistic interactions, nothing is known about the effects of P. aeruginosa and 65 S. aureus interactions in this context of coexisting bacteria within the same infectious niche. 66Using a transcriptomic approach, we analyzed how co-cultivation with non-competitive P. 67 aeruginosa altered S. aureus gene expression, especially genes encoding Nor family efflux 68 pumps. In the presence of P. aeruginosa, over-expression of these genes increased S. aureus 69 antibiotic tolerance and the rate of internalization into epithelial cells, two key determinants of 70 chronic infection. 71 72 5 RESULTS 73Coexistence interaction involves more than half of the S. aureus and P. aeruginosa isolates 74 from co-infected CF patients. 75Two types of interactions between S. aureus and P. aeruginosa could be observed with CF 76 patient isolates: the well-described competitive phenotype, where P. aeruginosa inhibits S. 77 aureus growth, 16 and the newly describe...

show abstract

Section: Discussionsupporting

confidence: 88%

Coexistence withPseudomonas aeruginosaaltersStaphylococcus aureustranscriptome, antibiotic resistance and internalization into epithelial cells

Briaud

Camus

Bastien

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…The RNAseq revealed two BK features related to metabolism: an up‐regulation of transporters and glycosidases, and a down‐regulation of translation‐related genes. tRNAs up‐regulation is a mechanism that allow bacteria in co‐cultures to grow better in a medium where there is competition for nutrients (Tognon, Köhler, Luscher, & van Delden, ). It is also a hallmark of cancer cells, where increased tRNAs can increase the translation of mRNA that bear their cognate codons (Goodarzi et al, ).…”

Section: Discussionmentioning

confidence: 99%

“…tRNAs up-regulation is a mechanism that allow bacteria in co-cultures to grow better in a medium where there is competition for nutrients (Tognon, Köhler, Luscher, & van Delden, 2019). It is also a hallmark of cancer cells, where increased tRNAs can increase the translation of mRNA that bear their cognate codons (Goodarzi et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Blind killing of both male and female Drosophila embryos by a natural variant of the endosymbiotic bacterium Spiroplasma poulsonii

Masson

Calderon-Copete²,

Schüpfer

et al. 2020

Cellular Microbiology

View full text Add to dashboard Cite

Spiroplasma poulsonii is a vertically transmitted endosymbiont of Drosophila melanogaster that causes male‐killing, that is the death of infected male embryos during embryogenesis. Here, we report a natural variant of S. poulsonii that is efficiently vertically transmitted yet does not selectively kill males, but kills rather a subset of all embryos regardless of their sex, a phenotype we call ‘blind‐killing’. We show that the natural plasmid of S. poulsonii has an altered structure: Spaid, the gene coding for the male‐killing toxin, is deleted in the blind‐killing strain, confirming its function as a male‐killing factor. Then we further investigate several hypotheses that could explain the sex‐independent toxicity of this new strain on host embryos. As the second non‐male‐killing variant isolated from a male‐killing original population, this new strain raises questions on how male‐killing is maintained or lost in fly populations. As a natural knock‐out of Spaid, which is unachievable yet by genetic engineering approaches, this variant also represents a valuable tool for further investigations on the male‐killing mechanism.

show abstract

“…42 Another set of genes that were differentially expressed encode a putative CidA/CidB-like, holin/anti-holin system (AK34_3040, AK34_3041) that was significantly downregulated (~64-and 42-fold, respectively) in B. dolosa carrying the evolved FixL variant (Supplemental Table 2). Homologs of this system were found to up-regulated in P. aeruginosa when grown in vitro with Staphylococcus aureus, 43 suggesting that upregulation of this system may result in more autolysis and increased biofilm formation. 44 Further investigation is needed to determine the role of these genes in BCC virulence and their role in fix pathwaymediated phenotypes.…”

Section: Discussionmentioning

confidence: 99%

Host adaptations in thefixLJpathway of theBurkholderia cepaciacomplex increase virulence

Schaefers

Wang

Boisvert

et al. 2020

Preprint

View full text Add to dashboard Cite

The Burkholderia cepacia complex (BCC) is composed of multiple species, including B. multivorans and B. dolosa, that are significant pathogens for people with cystic fibrosis (CF) and are extensively resistant to many antibiotics. The fixL gene of the fixLJ 2component system (TCS) in these BCC species shows evidence of positive selection for nonsynonymous mutations during chronic lung infection in CF. Previous work showed that the B. dolosa fixLJ system regulates 11% of the genome and modulates biofilm formation, motility, persistence within macrophages, and virulence in a murine pneumonia model. Here, we assess the impacts of clinically observed FixL evolved variants in fixLJ pathway-mediated phenotypes in B. dolosa and B. multivorans. BCC carrying the ancestral fixL sequence are less pathogenic than constructs carrying evolved variants in both a macrophage infection model and a murine pneumonia model. In vitro phospho-transfer experiments demonstrate that the evolved B. dolosa FixL variants are able to reduce fixLJ pathway activity by either having lower levels of kinase activity or increased phosphatase activity. Notably, the ancestral fixL genotype has increased ability to survive within the soil compared to isogenic constructs with evolved fixL genotypes, demonstrating that increased virulence comes at an expense. Modulation of the FixLJ system has profound effects on many BCC phenotypes including full pathogenicity, and this modulation is critical for BCC adaptation to the host. MainThe Burkholderia cepacia complex (BCC) is a group of more than 20 species of closelyrelated Gram-negative bacilli that can be dangerous respiratory pathogens for people with cystic fibrosis (CF). 1,2 Among CF patients in the US colonized with BCC, the species most commonly seen are B. cenocepacia and B. multivorans, although there is significant variability based on geographic region and institution, 3-7 and B. multivorans has emerged as the most predominant BCC species infecting CF patients in some regions. 4-7 BCC members have caused several outbreaks within the CF community, 2 including one outbreak of a highly antibiotic-resistant strain of B. dolosa among almost 40 CF patients in Boston 8 and another of B. cenocepacia in Toronto. 9 BCC can also cause serious infections in individuals with chronic granulomatous disease (CGD). 10 Outbreaks of hospital-acquired BCC infections in non-CF and non-CGD patients have also been increasingly described, often associated with contaminated medications, 11-16 including a recent outbreak associated with contamination of the stool softener docusate with B. contaminans. 15,16 Analysis of genomic diversity arising during B. dolosa and B. multivorans chronic infections in CF identified the fixLJ two-component system (TCS) as a pathway that is under positive selection, evident from enrichment for non-synonymous mutations as opposed to synonymous mutations and genetic parallelism among many independent infections. [17][18][19] TCSs are one mechanism that bacteria use to sense and respond to thei...

show abstract

Transcriptional profiling of Pseudomonas aeruginosa and Staphylococcus aureus during in vitro co-culture

Cited by 72 publications

References 57 publications

Coexistence withPseudomonas aeruginosaaltersStaphylococcus aureustranscriptome, antibiotic resistance and internalization into epithelial cells

Coexistence withPseudomonas aeruginosaaltersStaphylococcus aureustranscriptome, antibiotic resistance and internalization into epithelial cells

Blind killing of both male and female Drosophila embryos by a natural variant of the endosymbiotic bacterium Spiroplasma poulsonii

Host adaptations in thefixLJpathway of theBurkholderia cepaciacomplex increase virulence

Contact Info

Product

Resources

About