Bifidobacterium thermophilum RBL67 impacts on growth and virulence gene expression of Salmonella enterica subsp. enterica serovar Typhimurium. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Tanner, Sabine; Chassard, Christophe; Rigozzi, Eugenia; Lacroix, Christophe; Stevens, Marc
• Is Part Of: BMC microbiology. Volume 16:Issue 1(2016)
• Page Start: 1
• Page End: 16
• Publication Date: 2016-12
• Subjects: Bifidobacterium thermophilum -- Salmonella Typhimurium -- Co-culture -- RNA-seq -- Probiotic -- Anti-microbial -- Virulence; Microbiology -- Periodicals; 579.05
• DOI: 10.1186/s12866-016-0659-x
• Languages: English
• ISSNs: 1471-2180

Abstract

Abstract Background Bifidobacterium thermophilum RBL67 (RBL67), a human fecal isolate and health promoting candidate shows antagonistic and protective effects againstSalmonella andListeria spec. in vitro. However, the underlying mechanisms fostering these effects remain unknown. In this study, the interactions of RBL67 andSalmonella enterica subsp.enterica serovar Typhimurium N-15 (N-15) were explored by global transcriptional analysis. Results Growth experiments were performed in a complex nutritive medium with controlled pH of 6.0 and suitable for balanced growth of both RBL67 and N-15. RBL67 growth was slightly enhanced in presence of N-15. Conversely, N-15 showed reduced growth in the presence of RBL67. Transcriptional analyses revealed higher expression of stress genes and amino acid related function in RBL67 in co-culture with N-15 when compared to mono-culture. Repression of the PhoP regulator was observed in N-15 in presence of RBL67. Further, RBL67 activated virulence genes located on theSalmonella pathogenicity islands 1 and 2. Flagellar genes, however, were repressed by RBL67. Sequential expression of flagellar, SPI 1 and fimbrial genes is essential forSalmonella infection. Our data revealed that RBL67 triggers expression of SPI 1 and fimbrial determinants prematurely, potentially leading to redundant energy expenditure. In the competitive environment of the gut such energy expenditure could lead to enhanced clearing ofSalmonella . Conclusion Our study provides first insights into probiotic-pathogen interactions on global transcriptional level and suggests that deregulation of virulence gene expression might be an additional protective mechanism of probiotica against infections of the host.