ArticlePLoS pathogens2015
The νSaα Specific Lipoprotein Like Cluster (lpl) of S. aureus USA300 Contributes to Immune Stimulation and Invasion in Human Cells.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 76 citations in OpenAlex.
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- Targeting host-specific metabolic pathways-opportunities and challenges for anti-infective therapy.Frontiers in molecular biosciences · 2024Review
- A type VII-secreted lipase toxin with reverse domain arrangement.Nature communications · 2023Article
- GehB Inactivates Lipoproteins to Delay the Healing of Acute Wounds Infected with Staphylococcus aureus.Current microbiology · 2023Article
- Bacterial Lipoproteins Shift Cellular Metabolism to Glycolysis in Macrophages Causing Bone Erosion.Microbiology spectrum · 2023Article
- Complete Genome Sequence and Analysis of a ST573 Multidrug-Resistant Methicillin-ResistantPathogens (Basel, Switzerland) · 2023Article
- From an Hsp90 - binding protein to a peptide drug.microLife · 2023Article
- A genetic regulatory see-saw of biofilm and virulence in MRSA pathogenesis.Frontiers in microbiology · 2023Review
- Atopic dermatitis-derivedFrontiers in cellular and infection microbiology · 2023Article
- Keratinocytes use FPR2 to detectFrontiers in immunology · 2023Article
- The Influence of Antibiotic Resistance on Innate Immune Responses toAntibiotics (Basel, Switzerland) · 2022Review
- Review
Corrections and comments
- Erratum issuedCorrection: The νSaα Specific Lipoprotein Like Cluster (lpl) of S. aureus USA300 Contributes to Immune Stimulation and Invasion in Human Cells.2015 · Demicrioglu, Dogan Doruk [corrected to Demircioglu, Dogan Doruk]
Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
All Staphylococcus aureus genomes contain a genomic island, which is termed νSaα and characterized by two clusters of tandem repeat sequences, i.e. the exotoxin (set) and 'lipoprotein-like' genes (lpl). Based on their structural similarities the νSaα islands have been classified as type I to IV. The genomes of highly pathogenic and particularly epidemic S. aureus strains (USA300, N315, Mu50, NCTC8325, Newman, COL, JH1 or JH9) belonging to the clonal complexes CC5 and CC8 bear a type I νSaα island. Since the contribution of the lpl gene cluster encoded in the νSaα island to virulence is unclear to date, we deleted the entire lpl gene cluster in S. aureus USA300. The results showed that the mutant was deficient in the stimulation of pro-inflammatory cytokines in human monocytes, macrophages and keratinocytes. Purified lipoprotein Lpl1 was further shown to elicit a TLR2-dependent response. Furthermore, heterologous expression of the USA300 lpl cluster in other S. aureus strains enhanced their immune stimulatory activity. Most importantly, the lpl cluster contributed to invasion of S. aureus into human keratinocytes and mouse skin and the non-invasive S. carnosus expressing the lpl gene cluster became invasive. Additionally, in a murine kidney abscess model the bacterial burden in the kidneys was higher in wild type than in mutant mice. In this infection model the lpl cluster, thus, contributes to virulence. The present report is one of the first studies addressing the role of the νSaα encoded lpl gene cluster in staphylococcal virulence. The finding that the lpl gene cluster contributes to internalization into non-professional antigen presenting cells such as keratinocytes highlights the lpl as a new cell surface component that triggers host cell invasion by S. aureus. Increased invasion in murine skin and an increased bacterial burden in a murine kidney abscess model suggest that the lpl gene cluster serves as an important virulence factor.
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