Abstract
Pseudomonas aeruginosa is an ubiquitous gram-negative opportunistic human pathogen which is not considered part of the human commensal gut microbiota. However, depletion of the intestinal microbiota (Dysbiosis) following antibiotic treatment facilitates the colonization of the intestinal tract by Multidrug-Resistant P. aeruginosa. One possible strategy is based on the use of functional foods with prebiotic activity. The bifidogenic effect of the prebiotic inulin and its hydrolyzed form (fructooligosaccharide: FOS) is well established since they promote the growth of specific beneficial (probiotic) gut bacteria such as bifidobacteria. Previous studies of the opportunistic nosocomial pathogen Pseudomonas aeruginosa PAO1 have shown that inulin and to a greater extent FOS reduce growth and biofilm formation, which was found to be due to a decrease in motility and exotoxin secretion. However, the transcriptional basis for these phenotypic alterations remains unclear. To address this question we conducted RNA-sequence analysis. Changes in the transcript level induced by inulin and FOS were similar, but a set of transcript levels were increased in response to inulin and reduced in the presence of FOS. In the presence of inulin or FOS, 260 and 217 transcript levels, respectively, were altered compared to the control to which no polysaccharide was added. Importantly, changes in transcript levels of 57 and 83 genes were found to be specific for either inulin or FOS, respectively, indicating that both compounds trigger different changes. Gene pathway analyses of differentially expressed genes (DEG) revealed a specific FOS-mediated reduction in transcript levels of genes that participate in several canonical pathways involved in metabolism and growth, motility, biofilm formation, β-lactamase resistance, and in the modulation of type III and VI secretion systems; results that have been partially verified by real time quantitative PCR measurements. Moreover, we have identified a genomic island formed by a cluster of 15 genes, encoding uncharacterized proteins, which were repressed in the presence of FOS. The analysis of isogenic mutants has shown that genes of this genomic island encode proteins involved in growth, biofilm formation and motility. These results indicate that FOS selectively modulates bacterial pathogenicity by interfering with different signaling pathways.
Highlights
The human pathogen Pseudomonas aeruginosa causes a wide array of life-threatening acute and chronic infections, in immunocompromised, cancer, burn wound, and cystic fibrosis patients (Juhas, 2015)
In addition to the bacterial growth promoting role of inulin and FOS, we reported that FOS inhibited bacterial growth and biofilm formation of P. aeruginosa PAO1 (Ortega-González et al, 2014)
Between 5,300,000 and up to 7,500,000 reads were obtained for inuline and FOS respectively, of which approximately 85% could be assigned to the 6,322 coding regions of the P. aeruginosa PAO1 reference genome (Table 1)
Summary
The human pathogen Pseudomonas aeruginosa causes a wide array of life-threatening acute and chronic infections, in immunocompromised, cancer, burn wound, and cystic fibrosis patients (Juhas, 2015). This bacterium is one of the leading causes of nosocomial infections affecting hospitalized patients (Buhl et al, 2015) and mortality associated with hospitalacquired P. aeruginosa infectious like ventilator-associated pneumonia or bacteremia is above 35% (Lynch et al, 2017). This species is characterized by its ability to synthesize the virulent factors exotoxin A and pyocyanin (Ortiz-Castro et al, 2014) that block protein synthesis leading to cell death (Gaines et al, 2007)
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