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A role of epithelial cells and virulence factors in biofilm formation by Streptococcus pyogenes in vitro

Alamiri, Feiruz (author)
Lund University,Lunds universitet,Experimentell infektionsmedicin, Malmö,Forskargrupper vid Lunds universitet,Experimental Infection Medicine, Malmö,Lund University Research Groups
Chao, Yashuan (author)
Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Experimentell infektionsmedicin, Malmö,Forskargrupper vid Lunds universitet,Immunmodulerande effekter av blodplättar vid inflammation och infektion,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Experimental Infection Medicine, Malmö,Lund University Research Groups,Immunomodulatory effects of platelets during inflammation and infection
Baumgarten, Maria (author)
Lund University,Lunds universitet,Infektionsmedicin,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Infection Medicine (BMC),Section III,Department of Clinical Sciences, Lund,Faculty of Medicine
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Riesbeck, Kristian (author)
Lund University,Lunds universitet,Klinisk mikrobiologi, Malmö,Forskargrupper vid Lunds universitet,Clinical Microbiology, Malmö,Lund University Research Groups
Hakansson, Anders P (author)
Lund University,Lunds universitet,Experimentell infektionsmedicin, Malmö,Forskargrupper vid Lunds universitet,SEBRA Sepsis and Bacterial Resistance Alliance,Experimental Infection Medicine, Malmö,Lund University Research Groups
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 (creator_code:org_t)
2020
2020
English.
In: Infection and Immunity. - 1098-5522. ; 88:10
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Biofilm formation by Streptococcus pyogenes (GAS) in model systems mimicking the respiratory tract is poorly documented. Most studies have been conducted on abiotic surfaces, which poorly represent human tissues. We have previously shown that GAS forms mature and antibiotic-resistant biofilms on physiologically relevant epithelial cells. However, the role of the substratum, extracellular matrix (ECM) components, or GAS virulence factors for biofilm formation and structure is unclear. In this study, biofilm formation was measured on respiratory epithelial cells and keratinocytes by determining biomass and antibiotic resistance, and biofilm morphology was visualized using scanning electron microscopy. All GAS isolates tested formed biofilms that had similar, albeit not identical, biomass and antibiotic resistance for both cell types. Interestingly, functionally mature biofilms formed more rapidly on keratinocytes but were structurally denser and coated with more ECM on respiratory epithelial cells. The ECM was crucial for biofilm integrity, as protein- and DNA-degrading enzymes induced bacterial release from biofilms. Abiotic surfaces supported biofilm formation, but these biofilms were structurally less dense and organized. No major role of M protein, capsule, or Streptolysin O was observed in biofilm formation on epithelial cells, although some morphological differences were detected. NAD-glycohydrolase was required for optimal biofilm formation, whereas Streptolysin S or cysteine protease SpeB impaired this process. Finally, no correlation was found between cell adherence or auto-aggregation and GAS biofilm formation. Combined, these results provide a better understanding of the role of biofilm formation in GAS pathogenesis and can potentially provide novel targets for future treatments against GAS infections.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Infektionsmedicin (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Infectious Medicine (hsv//eng)

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