The Maternal Group B Streptococcus Alpha-Like Protein Subunit Vaccine GBS-NN Targets Homotypic and Heterotypic Strains, Confers Opsonophagocytic Killing and Prevents in vitro Invasion of Human Epithelial Cells

2021 ◽  
Author(s):  
Andrzej Pawlowski ◽  
Jonas Lannergård ◽  
Majela Gonzalez-Miro ◽  
Duojia Cao ◽  
Sara Larsson ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Subunit Vaccine ◽  
Group B Streptococcus ◽  
Protein Subunit ◽  
Human Epithelial Cells ◽  
Group B ◽  
Opsonophagocytic Killing

scholarly journals Oxygen Regulates Invasiveness and Virulence of Group B Streptococcus

2003 ◽  
Vol 71 (12) ◽  
pp. 6707-6711 ◽  
Author(s):  
Atul K. Johri ◽  
Joahnna Padilla ◽  
Gennady Malin ◽  
Lawrence C. Paoletti
Keyword(s):  
Epithelial Cells ◽  
Cell Mass ◽  
Group B Streptococcus ◽  
Positive Association ◽  
The Elderly ◽  
Opportunistic Pathogen ◽  
Human Epithelial Cells ◽  
Group B ◽  
In Vitro Invasiveness

ABSTRACT The facultative anaerobe group B Streptococcus (GBS) is an opportunistic pathogen of pregnant women, newborns, and the elderly. Although several virulence factors have been identified, environmental factors that regulate the pathogenicity of GBS have not been well characterized. Using the dynamic in vitro attachment and invasion system (DIVAS), we examined the effect of oxygen on the ability of GBS to invade immortalized human epithelial cells. GBS type III strain M781 invaded human epithelial cells of primitive neurons, the cervix, the vagina, and the endometrium in 5- to 400-fold higher numbers when cultured at a cell mass doubling time (td ) of 1.8 h than at a slower td of 11 h. Invasion was optimal when GBS was cultured at a td of 1.8 h in the presence of ≥5% oxygen and was significantly reduced without oxygen. Moreover, GBS grown in a chemostat under highly invasive conditions (td of 1.8 h, with oxygen) was more virulent in neonatal mice than was GBS grown under suboptimal invasion conditions (td of 1.8 h, without oxygen), suggesting a positive association between in vitro invasiveness with DIVAS and virulence.

A cytosol derived factor of Group B streptococcus prevent its invasion into human epithelial cells

2018 ◽  
Vol 34 (3) ◽  
Author(s):  
Manju Ohri ◽  
Smriti Parashar ◽  
Venkatesh S. Pai ◽  
Sujata Ghosh ◽  
Anuradha Chakraborti
Keyword(s):  
Epithelial Cells ◽  
Group B Streptococcus ◽  
Human Epithelial Cells ◽  
Group B

scholarly journals Human milk oligosaccharides reduce murine group B Streptococcus vaginal colonization with minimal impact on the vaginal microbiota

2021 ◽  
Author(s):  
Marlyd E Mejia ◽  
Samantha Ottinger ◽  
Alison Vrbanac ◽  
Priyanka Babu ◽  
Jacob Zulk ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Human Milk ◽  
Biofilm Formation ◽  
Group B Streptococcus ◽  
Human Milk Oligosaccharides ◽  
Vaginal Colonization ◽  
Vaginal Epithelial Cells ◽  
Group B

Group B Streptococcus (GBS) colonizes the vaginal mucosa of a significant percentage of healthy women and is a leading cause of neonatal bacterial infections. Currently, pregnant women are screened in the last month of pregnancy and GBS-positive women are given antibiotics during parturition to prevent bacterial transmission to the neonate. Recently, human milk oligosaccharides (HMOs) isolated from breastmilk were found to inhibit GBS growth and biofilm formation in vitro, and women that make certain HMOs are less likely to be vaginally colonized with GBS. Using in vitro human vaginal epithelial cells and a murine vaginal colonization model, we tested the impact of HMO treatment on GBS burdens and the composition of the endogenous microbiota by 16S rRNA amplicon sequencing. HMO treatment reduced GBS vaginal burdens in vivo with minimal alterations to the vaginal microbiota. HMOs displayed potent inhibitory activity against GBS in vitro, but HMO pretreatment did not alter adherence of GBS or the probiotic Lactobacillus rhamnosus to human vaginal epithelial cells. Additionally, disruption of a putative GBS glycosyltransferase (Δsan_0913) rendered the bacterium largely resistant to HMO inhibition in vitro and in vivo but did not compromise its adherence, colonization, or biofilm formation in the absence of HMOs. We conclude that HMOs are a promising therapeutic bioactive to limit GBS vaginal colonization with minimal impacts on the vaginal microenvironment.

scholarly journals BsaB, a Novel Adherence Factor of Group B Streptococcus

2013 ◽  
Vol 82 (3) ◽  
pp. 1007-1016 ◽  
Author(s):  
Shengmei Jiang ◽  
Michael R. Wessels
Keyword(s):  
Extracellular Matrix ◽  
Epithelial Cells ◽  
Group B Streptococcus ◽  
Surface Protein ◽  
Chronically Ill ◽  
Host Cells ◽  
Upstream Open Reading Frame ◽  
Content Type ◽  
Group B

ABSTRACTStreptococcus agalactiae(group BStreptococcus[GBS]) is a leading cause of neonatal sepsis and meningitis, peripartum infections in women, and invasive infections in chronically ill or elderly individuals. GBS can be isolated from the gastrointestinal or genital tracts of up to 30% of healthy adults, and infection is thought to arise from invasion from a colonized mucosal site. Accordingly, bacterial surface components that mediate attachment of GBS to host cells or the extracellular matrix represent key factors in the colonization and infection of the human host. We identified a conserved GBS gene of unknown function that was predicted to encode a cell wall-anchored surface protein. Deletion of the gene and a cotranscribed upstream open reading frame (ORF) in GBS strain 515 reduced bacterial adherence to VK2 vaginal epithelial cellsin vitroand reduced GBS binding to fibronectin-coated microtiter wells. Expression of the gene product inLactococcus lactisconferred the ability to adhere to VK2 cells, to fibronectin and laminin, and to fibronectin-coated ME-180 cervical epithelial cells. Expression of the recombinant protein inL. lactisalso markedly increased biofilm formation. The adherence function of the protein, namedbacterialsurfaceadhesin of GBS (BsaB), depended both on a central BID1 domain found in bacterial intimin-like proteins and on the C-terminal portion of the BsaB protein. Expression of BsaB in GBS, like that of several other adhesins, was regulated by the CsrRS two-component system. We conclude that BsaB represents a newly identified adhesin that participates in GBS attachment to epithelial cells and the extracellular matrix.

Metallothionein in cultured human epithelial cells and synovial rheumatoid fibroblasts after in vitro treatment with auranofin

1986 ◽  
Vol 35 (12) ◽  
pp. 2033-2040 ◽  
Author(s):  
Anne Glennås ◽  
Peter E. Hunziker ◽  
Justine S. Garvey ◽  
Jeremias H.R. Kägi ◽  
Hans E. Rugstad
Keyword(s):  
Epithelial Cells ◽  
Human Epithelial Cells ◽  
In Vitro Treatment

Group B Streptococcal and Pneumococcal Sepsis in Newborn Infants: The Role of Pneumococcal Antibody

PEDIATRICS ◽  
1978 ◽  
Vol 62 (4) ◽  
pp. 620-621
Author(s):  
Gerald W. Fischer ◽  
James W. Bass ◽  
George H. Lowell ◽  
Martin H. Crumrine
Keyword(s):  
Streptococcus Pneumoniae ◽  
Hydrochloric Acid ◽  
Group B Streptococcus ◽  
Newborn Infants ◽  
Polysaccharide Antigen ◽  
Type Iii ◽  
Pneumococcal Sepsis ◽  
Group B

The article by Bortolussi et al. on pneumococcal septicemia and meningitis in the neonat (Pediatrics 60:352, September 1977) was of great interest to us, since we have been analyzing the effect of antibody directed against Streptococcus pneumoniae on group B Streptococcus type III. We have recently shown (unpublished data) that antibody directed against S. pneumoniae type 14 precipitates the hot hydrochloric acid-extracted polysaccharide antigen of group B Streptococcus type III. Further studies have shown that this antibody is opsonic for group B Streptococcus type III in an in vitro bactericidal assay and protective in a suckling rat model of group B Streptococcus type III sepsis.1

scholarly journals In vitro modeling of the interaction between human epithelial cells and lymphocytes upon influenza infection

2016 ◽  
Vol 10 (5) ◽  
pp. 438-442 ◽  
Author(s):  
Natalia A. Ilyushina ◽  
Peter F. Wright
Keyword(s):  
Epithelial Cells ◽  
Influenza Infection ◽  
In Vitro Modeling ◽  
Human Epithelial Cells
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