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Infection of endothelial cells by Streptococcus agalactiae reveals potential role of PI-2b pilus on endothelial
Jessica Silva Santos de Oliveira1, Bruna Alves da Silva Pimentel1, Leonardo Nagao Ferreira2
1Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcantara Gomes, Laboratório de Biologia Molecular e Fisiologia de Estreptococos, Rio de Janeiro, RJ, Brasil.
Background:
Streptococcus agalactiae is responsible for sepsis and meningitis, and the major cause of neonatal morbidity and mortality. However, how S. agalactiae disrupts endothelial barriers is poorly understood.
Objectives:
Analyse the influence of endothelial cell (HUVECs) growth under static and shear stress conditions during infection with S. agalactiae, and the role of pilus PI-2b during endothelial barrier disruption and increased endothelial permeability.
Methods:
HUVECs under static and shear conditions were infected by S. agalactiae (GBS90356 and GBS90356Δpilus2b) strains in the presence and absence of fibrinogen. VE-cadherin was evaluated by immunofluorescence and RT-PCR assays, and the endothelial permeability by transwell assay.
Finds:
Shear stress induced the alignment of HUVECs and increased the adherence of S. agalactiae strains (GBS90356 and GBS90356Δpilus2b), mainly in the presence of fibrinogen, in addition to greater peripheral localisation of VE-cadherin. Rupture points and damage to endothelial integrity was visualised after infection with the GBS90356WT strain, mainly in the presence of fibrinogen. RT-PCR analyses identified increase in VE-cadherin expression in HUVECs under shear stress and a decrease in VE-cadherin after infection, with increased levels of endothelial permeability.
Main Conclusion:
Data demonstrate for the first time the dysfunction of the adhesive barrier induced by the S. agalactiae ST-17 strain, mainly in HUVECs under shear stress, where PI-2b expression was essential to optimise the damage to endothelial integrity.
Insights
Streptococcus agalactiae infection damages endothelial barriers, especially under shear stress. The pilus PI-2b is crucial for this bacterial disruption of the endothelial cell lining.
Area of Science:
- Microbiology and Immunology
- Cell Biology
- Vascular Biology
Background:
- Streptococcus agalactiae causes neonatal sepsis and meningitis.
- The mechanism of endothelial barrier disruption by S. agalactiae is not well understood.
Purpose of the Study:
- To investigate how S. agalactiae affects endothelial cells (HUVECs) under static and shear stress.
- To determine the role of pilus PI-2b in endothelial barrier disruption and permeability.
Main Methods:
- Infection of HUVECs with S. agalactiae strains (wild-type and Δpilus2b) under static and shear conditions, with and without fibrinogen.
- Evaluation of VE-cadherin by immunofluorescence and RT-PCR.
- Assessment of endothelial permeability using transwell assays.
Main Results:
- Shear stress aligned HUVECs and increased bacterial adherence, particularly with fibrinogen.
- S. agalactiae infection, especially the wild-type strain with fibrinogen, caused endothelial damage and rupture points.
- VE-cadherin expression increased under shear stress but decreased post-infection, correlating with increased endothelial permeability.
Conclusions:
- S. agalactiae ST-17 disrupts the endothelial adhesive barrier, particularly in HUVECs under shear stress.
- Pilus PI-2b expression is essential for S. agalactiae to effectively damage endothelial integrity.
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