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The νSaα Specific Lipoprotein Like Cluster () of . USA300 Contributes to Immune Stimulation and Invasion in Human Cells


Highly pathogenic and epidemic Staphylococcus aureus strains carry a pathogenicity island in their genome that contains a cluster of lipoprotein-encoding genes termed lpl. As the role lpl in virulence is still unclear, we deleted the entire lpl cluster in the community-acquired methicillin-resistant S. aureus (CA-MRSA) USA300 and found that the mutant was defective in stimulation of pro-inflammatory cytokines in human immune cells. Moreover, the major finding highlighted in this study is that the lpl cluster contributes to invasion into non-professional phagocytes such as epithelial cells and keratinocytes. Furthermore, the lpl-dependent increase in invasive activity, most likely, accounts for the enhanced bacterial burden observed in a murine kidney abscess model. In general, internalization of a pathogen into host epithelial cells shields the pathogen from immune defense and antibiotic treatment. However, further investigation is needed to clarify whether the increased ability to invade host cells is responsible for the potent disseminative activity and hypervirulent phenotype characterizing the νSaα type I island expressing S. aureus strains, including the USA300 CA-MRSA strain.


Vyšlo v časopise: The νSaα Specific Lipoprotein Like Cluster () of . USA300 Contributes to Immune Stimulation and Invasion in Human Cells. PLoS Pathog 11(6): e32767. doi:10.1371/journal.ppat.1004984
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004984

Souhrn

Highly pathogenic and epidemic Staphylococcus aureus strains carry a pathogenicity island in their genome that contains a cluster of lipoprotein-encoding genes termed lpl. As the role lpl in virulence is still unclear, we deleted the entire lpl cluster in the community-acquired methicillin-resistant S. aureus (CA-MRSA) USA300 and found that the mutant was defective in stimulation of pro-inflammatory cytokines in human immune cells. Moreover, the major finding highlighted in this study is that the lpl cluster contributes to invasion into non-professional phagocytes such as epithelial cells and keratinocytes. Furthermore, the lpl-dependent increase in invasive activity, most likely, accounts for the enhanced bacterial burden observed in a murine kidney abscess model. In general, internalization of a pathogen into host epithelial cells shields the pathogen from immune defense and antibiotic treatment. However, further investigation is needed to clarify whether the increased ability to invade host cells is responsible for the potent disseminative activity and hypervirulent phenotype characterizing the νSaα type I island expressing S. aureus strains, including the USA300 CA-MRSA strain.


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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

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