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Infection of endothelial cells by Streptococcus agalactiae reveals potential role of PI-2b pilus on endothelial barrier dysfunction.
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de Oliveira Jessica Silva Santos, Pimentel Bruna Alves da Silva, Ferreira Leonardo Nagao, Negreiro E Silva Maria Eduarda, Santos Gabriela da Silva, Nagao Prescilla Emy
Аннотация
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.
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.