A role of epithelial cells and virulence factors in biofilm formation by Streptococcus pyogenes in vitro
(2020) In Infection and Immunity 88(10).- Abstract
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... (More)
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.
(Less)
- author
- Alamiri, Feiruz
LU
; Chao, Yashuan
LU
; Baumgarten, Maria
LU
; Riesbeck, Kristian
LU
and Hakansson, Anders P LU
- organization
- publishing date
- 2020-09-18
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Infection and Immunity
- volume
- 88
- issue
- 10
- article number
- e00133-20
- publisher
- American Society for Microbiology
- external identifiers
-
- pmid:32661124
- scopus:85091324491
- ISSN
- 1098-5522
- DOI
- 10.1128/IAI.00133-20
- language
- English
- LU publication?
- yes
- additional info
- Copyright © 2020 American Society for Microbiology.
- id
- 72357db2-2d89-421e-8108-673b54013b25
- date added to LUP
- 2020-07-19 21:42:30
- date last changed
- 2024-05-29 17:02:25
@article{72357db2-2d89-421e-8108-673b54013b25, abstract = {{<p>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.</p>}}, author = {{Alamiri, Feiruz and Chao, Yashuan and Baumgarten, Maria and Riesbeck, Kristian and Hakansson, Anders P}}, issn = {{1098-5522}}, language = {{eng}}, month = {{09}}, number = {{10}}, publisher = {{American Society for Microbiology}}, series = {{Infection and Immunity}}, title = {{A role of epithelial cells and virulence factors in biofilm formation by Streptococcus pyogenes in vitro}}, url = {{http://dx.doi.org/10.1128/IAI.00133-20}}, doi = {{10.1128/IAI.00133-20}}, volume = {{88}}, year = {{2020}}, }