Abstract
Virulence factors, such as staphylococcal enterotoxin A (SEA), are contained within membrane vesicles (MVs) in the cell membrane of Staphylococcus aureus. In this study, the effects of the growth stage on quantitative and qualitative changes in the components contained in the MVs of S. aureus SEA-producing strains were examined. Changes in the expression levels of S. aureus genes were examined at each growth stage; phenol-soluble modulin (PSM) gene reached a maximum after 8 h, and the expression of cell membrane-related genes was decreased after 6 h. Based on these gene expression patterns, MVs were prepared at 6, 17, and 24 h. The particle size of MVs did not change depending on the growth stage. MVs prepared after culture for 17 h maintained their particle size when stored at 23 °C. The amount of SEA in the culture supernatant and MVs were not correlated. Bifunctional autolysin, a protein involved in cell wall biosynthesis/degradation, was increased in MVs at 17 h. The expression pattern of inflammation-related genes in human adult low calcium high temperature (HaCaT) cells induced by MVs was different for each growth stage. The inclusion components of S. aureus-derived MVs are selective, depend on the stage of growth, and may play an important role in toxicity.
Highlights
Publisher’s Note: MDPI stays neutralStaphylococcus aureus produces a variety of toxins and extracellular proteins, including staphylococcal enterotoxins (SEs), and causes various diseases, such as sepsis [1], pneumonia, and skin infections [2]
In membrane vesicles (MVs), considering that release and destruction occur at the same time and that there is an inclusion mechanism of selective virulence factors, it is possible that the properties of MVs may differ at each growth stage
To demonstrate that the properties of MVs may differ at each growth stage, MVs were prepared at 6, 17, and 24 h
Summary
Staphylococcus aureus produces a variety of toxins and extracellular proteins, including staphylococcal enterotoxins (SEs), and causes various diseases, such as sepsis [1], pneumonia, and skin infections [2]. Staphylococcal food poisoning, which is a typical disease, is caused by the ingestion of SEs released from S. aureus growing in food [3]. More than 20 types of SE have been reported, there are many cases of food poisoning due to enterotoxin A (SEA) worldwide [4]. Most SE production is regulated by the accessory gene regulator (agr), but the regulatory mechanism of SEA is at least partially associated with the lysogenic phage life cycle [5–7]. SEA production is not expected to correlate with culture time or the bacterial count. The genes encoding SEA are on the bacteriophage genome and their life cycle is characterized by two stages: lysogenic and lytic [8]
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