Abstract
Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCCmec. We previously found that SCCmec-encoded psm-mec RNA suppresses exotoxin production as a regulatory RNA, and the psm-mec translation product increases biofilm formation in Staphylococcus aureus. Here, we examined whether the regulatory role of psm-mec on host bacterial virulence properties is conserved among other staphylococcal species, S. epidermidis and S. haemolyticus, both of which are important causes of nosocomial infections. In S. epidermidis, introduction of psm-mec decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation. Introduction of psm-mec with a stop-codon mutation that did not express PSM-mec protein but did express psm-mec RNA also decreased PSM production, but did not increase biofilm formation. Thus, the psm-mec RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in S. epidermidis. In S. haemolyticus, introduction of psm-mec decreased PSM production, but did not affect biofilm formation. The mutated psm-mec with a stop-codon also caused the same effect. Thus, the psm-mec RNA also inhibits PSM production in S. haemolyticus. These findings suggest that the inhibitory role of psm-mec RNA on exotoxin production is conserved among staphylococcal species, although the stimulating effect of the psm-mec gene on biofilm formation is not conserved.
Highlights
Pathogenic bacteria produce exotoxins that damage host immune cells to facilitate bacterial survival and proliferation in the host environment
Results and Discussion psm-mec Alters the Virulence Phenotype of S. epidermidis To examine whether the alteration of the S. epidermidis phenotype by psm-mec is caused by the transcription product or the translation product of psm-mec, we transformed S. epidermidis with psm-mec carrying either a stop codon mutation or a deficient promoter, which we previously used in S. aureus [8] (Fig. 1A)
In this study, we revealed that the inhibitory effect of the psm-mec transcript against exotoxin production is conserved in S. epidermidis and S. haemolyticus
Summary
Pathogenic bacteria produce exotoxins that damage host immune cells to facilitate bacterial survival and proliferation in the host environment. Pathogenic bacteria form a biofilm to resist host immune factors and antibiotics [1]. Understanding the molecular mechanisms of exotoxin production and biofilm formation is important for establishing therapeutic strategies against infectious bacterial diseases. Bacteria possess virulence factors encoded on the core genome and acquire virulence factors by incorporating plasmids, phages, or transposons, which are known as mobile genetic elements [2]. Mobile genetic elements encode various virulence factors such as exotoxins and superantigens that directly interact with host factors [3,4]. Mobile genetic elements encode a regulatory factor against core genome encoded-virulence genes [5,6,7]
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