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Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation

Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Puls...

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Autores principales: Anderson, Michele J., Lin, Ying-Chi, Gillman, Aaron N., Parks, Patrick J., Schlievert, Patrick M., Peterson, Marnie L.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Research Foundation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417397/
https://www.ncbi.nlm.nih.gov/pubmed/22919655
http://dx.doi.org/10.3389/fcimb.2012.00064
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author Anderson, Michele J.
Lin, Ying-Chi
Gillman, Aaron N.
Parks, Patrick J.
Schlievert, Patrick M.
Peterson, Marnie L.
author_facet Anderson, Michele J.
Lin, Ying-Chi
Gillman, Aaron N.
Parks, Patrick J.
Schlievert, Patrick M.
Peterson, Marnie L.
author_sort Anderson, Michele J.
collection PubMed
description Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Pulsed-field gel electrophoresis clonal type USA200 is the most widely disseminated colonizer and the leading cause of TSS. The cytolysin α-toxin (also known as α-hemolysin or Hla) is the major epithelial proinflammatory exotoxin produced by TSS S. aureus USA200 isolates. The current study aims to characterize the differences between TSS USA200 strains [high (hla(+)) and low (hla(−)) α-toxin producers] in their ability to disrupt vaginal mucosal tissue and to characterize the subsequent infection. Tissue viability post-infection and biofilm formation of TSS USA200 isolates CDC587 and MN8, which contain the α-toxin pseudogene (hla(−)), MNPE (hla(+)), and MNPE isogenic hla knockout (hlaKO), were observed via LIVE/DEAD® staining and confocal microscopy. All TSS strains grew to similar bacterial densities (1–5 × 10(8) CFU) on the mucosa and were proinflammatory over 3 days. However, MNPE formed biofilms with significant reductions in the mucosal viability whereas neither CDC587 (hla(−)), MN8 (hla(−)), nor MNPE hlaKO formed biofilms. The latter strains were also less cytotoxic than wild-type MNPE. The addition of exogenous, purified α-toxin to MNPE hlaKO restored the biofilm phenotype. We speculate that α-toxin affects S. aureus phenotypic growth on vaginal mucosa by promoting tissue disruption and biofilm formation. Further, α-toxin mutants (hla(−)) are not benign colonizers, but rather form a different type of infection, which we have termed high density pathogenic variants (HDPV).
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spelling pubmed-34173972012-08-23 Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation Anderson, Michele J. Lin, Ying-Chi Gillman, Aaron N. Parks, Patrick J. Schlievert, Patrick M. Peterson, Marnie L. Front Cell Infect Microbiol Microbiology Staphylococcus aureus causes many diseases in humans, ranging from mild skin infections to serious, life-threatening, superantigen-mediated Toxic Shock Syndrome (TSS). S. aureus may be asymptomatically carried in the anterior nares or vagina or on the skin, serving as a reservoir for infection. Pulsed-field gel electrophoresis clonal type USA200 is the most widely disseminated colonizer and the leading cause of TSS. The cytolysin α-toxin (also known as α-hemolysin or Hla) is the major epithelial proinflammatory exotoxin produced by TSS S. aureus USA200 isolates. The current study aims to characterize the differences between TSS USA200 strains [high (hla(+)) and low (hla(−)) α-toxin producers] in their ability to disrupt vaginal mucosal tissue and to characterize the subsequent infection. Tissue viability post-infection and biofilm formation of TSS USA200 isolates CDC587 and MN8, which contain the α-toxin pseudogene (hla(−)), MNPE (hla(+)), and MNPE isogenic hla knockout (hlaKO), were observed via LIVE/DEAD® staining and confocal microscopy. All TSS strains grew to similar bacterial densities (1–5 × 10(8) CFU) on the mucosa and were proinflammatory over 3 days. However, MNPE formed biofilms with significant reductions in the mucosal viability whereas neither CDC587 (hla(−)), MN8 (hla(−)), nor MNPE hlaKO formed biofilms. The latter strains were also less cytotoxic than wild-type MNPE. The addition of exogenous, purified α-toxin to MNPE hlaKO restored the biofilm phenotype. We speculate that α-toxin affects S. aureus phenotypic growth on vaginal mucosa by promoting tissue disruption and biofilm formation. Further, α-toxin mutants (hla(−)) are not benign colonizers, but rather form a different type of infection, which we have termed high density pathogenic variants (HDPV). Frontiers Research Foundation 2012-05-09 /pmc/articles/PMC3417397/ /pubmed/22919655 http://dx.doi.org/10.3389/fcimb.2012.00064 Text en Copyright © 2012 Anderson, Lin, Gillman, Parks, Schlievert and Peterson. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.
spellingShingle Microbiology
Anderson, Michele J.
Lin, Ying-Chi
Gillman, Aaron N.
Parks, Patrick J.
Schlievert, Patrick M.
Peterson, Marnie L.
Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title_full Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title_fullStr Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title_full_unstemmed Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title_short Alpha-Toxin Promotes Staphylococcus aureus Mucosal Biofilm Formation
title_sort alpha-toxin promotes staphylococcus aureus mucosal biofilm formation
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3417397/
https://www.ncbi.nlm.nih.gov/pubmed/22919655
http://dx.doi.org/10.3389/fcimb.2012.00064
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