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 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.

scholarly journals Subtractive Hybridization Identifies a Novel Predicted Protein Mediating Epithelial Cell Invasion by Virulent Serotype III Group B Streptococcus agalactiae

2003 ◽  
Vol 71 (12) ◽  
pp. 6857-6863 ◽  
Author(s):  
Elisabeth E. Adderson ◽  
Shinji Takahashi ◽  
Yan Wang ◽  
Jianling Armstrong ◽  
Dylan V. Miller ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Streptococcus Agalactiae ◽  
Group B Streptococcus ◽  
Newborn Infants ◽  
Subtractive Hybridization ◽  
Group B Streptococci ◽  
Mutant Type ◽  
Isogenic Mutant ◽  
Type Iii ◽  
Group B

ABSTRACT Group B Streptococcus agalactiae bacteria (group B streptococci [GBS]) are the most common cause of serious bacterial infection in newborn infants. The majority of serotype III-related cases of neonatal disease are caused by a genetically related subgroup of bacteria, restriction fragment digest pattern (RDP) type III-3, suggesting that these strains possess unique genes contributing to virulence. We used genomic subtractive hybridization to identify regions of genomic DNA unique to virulent RDP type III-3 GBS strains. Within one of these III-3-specific regions is a 1,506-bp open reading frame, spb1 (surface protein of group B streptococcus 1). A mutant type III GBS strain lacking Spb1 was constructed in virulent RDP type III-3 strain 874391, and the interactions of the wild-type and spb1 isogenic mutant with a variety of epithelial cells important to GBS colonization and infection were compared. While adherence of the spb1 isogenic mutant to A549 respiratory, C2Bbe1 colonic, and HeLa cervical epithelial cells was slightly lower than that of the 874391 strain, invasion of the Spb1− mutant was significantly reduced with these cell lines compared to what was seen with 874391. The defect in epithelial invasion was corrected by supplying spb1 in trans. These observations suggest that Spb1 contributes to the pathogenesis of neonatal GBS infection by mediating internalization of virulent serotype III GBS and confirm that understanding of the population structure of bacteria may lead to insights into the pathogenesis of human infections.

Group B streptococcus alters properties of vaginal epithelial cells in pregnant women

2016 ◽  
Vol 214 (3) ◽  
pp. 383.e1-383.e5 ◽  
Author(s):  
Jessica Scholl ◽  
Dimitrios Nasioudis ◽  
Allison Boester ◽  
Maureen Speleotes ◽  
Amos Grunebaum ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Pregnant Women ◽  
Group B Streptococcus ◽  
Vaginal 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 The surface protein HvgA mediates group B streptococcus hypervirulence and meningeal tropism in neonates

2010 ◽  
Vol 207 (11) ◽  
pp. 2313-2322 ◽  
Author(s):  
Asmaa Tazi ◽  
Olivier Disson ◽  
Samuel Bellais ◽  
Abdelouhab Bouaboud ◽  
Nicolas Dmytruk ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Late Onset ◽  
Group B Streptococcus ◽  
Intestinal Barrier ◽  
Surface Protein ◽  
Oral Route ◽  
Neonatal Meningitis ◽  
Promising Target ◽  
Single Clone ◽  
Group B

Streptococcus agalactiae (group B streptococcus; GBS) is a normal constituent of the intestinal microflora and the major cause of human neonatal meningitis. A single clone, GBS ST-17, is strongly associated with a deadly form of the infection called late-onset disease (LOD), which is characterized by meningitis in infants after the first week of life. The pathophysiology of LOD remains poorly understood, but our epidemiological and histopathological results point to an oral route of infection. Here, we identify a novel ST-17–specific surface-anchored protein that we call hypervirulent GBS adhesin (HvgA), and demonstrate that its expression is required for GBS hypervirulence. GBS strains that express HvgA adhered more efficiently to intestinal epithelial cells, choroid plexus epithelial cells, and microvascular endothelial cells that constitute the blood–brain barrier (BBB), than did strains that do not express HvgA. Heterologous expression of HvgA in nonadhesive bacteria conferred the ability to adhere to intestinal barrier and BBB-constituting cells. In orally inoculated mice, HvgA was required for intestinal colonization and translocation across the intestinal barrier and the BBB, leading to meningitis. In conclusion, HvgA is a critical virulence trait of GBS in the neonatal context and stands as a promising target for the development of novel diagnostic and antibacterial strategies.

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.

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