scholarly journals Phenotypic changes in group B streptococci grown in the presence of the polyols, erythritol, sorbitol and mannitol

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Maram Hulbah ◽  
Matthew A. Croxen ◽  
Gregory J. Tyrrell
Keyword(s):  
Epithelial Cell ◽  
Amniotic Fluid ◽  
Biofilm Formation ◽  
Surface Expression ◽  
Invasive Disease ◽  
Epithelial Cell Line ◽  
Sugar Alcohols ◽  
Group B Streptococci ◽  
Phenotypic Changes ◽  
Group B

Abstract Background Group B streptococci (GBS) are important neonatal bacterial pathogens that can cause severe invasive disease in the newborn. It is thought that in many cases of invasive neonatal GBS disease, the bacteria ascend the vagina into the uterus and infect the amniotic fluid surrounding the fetus. Important constituents of this environment include the polyols or sugar alcohols of which erythritol, sorbitol and mannitol are examples. The aim of our study was to investigate the effect of polyols on GBS grown in media containing these sugar alcohols. Results GBS incubated in varying concentrations of polyols (erythritol, sorbitol or mannitol) did not display any significant enhancement or inhibition of bacterial growth. However, growth of GBS in the presence of erythritol significantly increased the surface expression of GBS-PGK (a plasminogen binding protein) 1.25 to 1.5-fold depending on the erythritol concentration and significantly enhanced the survival in human blood 3X to 18X depending on the concentration of polyol used. Interestingly, GBS grown in 1% erythritol significantly increased invasion by the bacteria of HeLa cells (epithelial cell line) (150% vs 100%) however, at higher concentrations (2% or 4% of polyol) the number of CFUs was significantly reduced (55-75% vs 100%) suggesting higher concentrations of polyols may inhibit invasion. Erythritol also increased GBS hemolytic activity as well as enhancing biofilm formation 1.4X to 3.3X depending on the concentration of polyol used. Conclusions GBS grown in the presence of polyols alters the bacteria’s phenotype resulting in changes associated with GBS virulence. This effect was greatest for the polyol erythritol.

scholarly journals A unique serine-rich repeat protein (Srr-2) and novel surface antigen (ε) associated with a virulent lineage of serotype III Streptococcus agalactiae

Microbiology ◽  
2006 ◽  
Vol 152 (4) ◽  
pp. 1029-1040 ◽  
Author(s):  
Kyle N. Seifert ◽  
Elisabeth E. Adderson ◽  
April A. Whiting ◽  
John F. Bohnsack ◽  
Paula J. Crowley ◽  
...  
Keyword(s):  
Surface Antigen ◽  
Invasive Disease ◽  
Group B Streptococci ◽  
Gene Encoding ◽  
Repeat Protein ◽  
Encoding Gene ◽  
Group B ◽  
Mouse Model Of Infection ◽  
Highly Virulent

Group B streptococci (GBS) are pathogens of both neonates and adults, with serotype III strains in particular being associated with invasive disease and meningitis. In this study, a novel GBS surface antigen, ε, was found to be co-expressed with the previously reported δ antigen on an identical subset of serotype III GBS. Expression of δ/ε on the surface of serotype III GBS was shown to distinguish the restriction digest pattern (RDP) III-3 and multilocus sequence typing (ST)-17 lineage. ε-Specific antibodies were reactive with a unique, high-molecular-mass, serine-rich repeat protein (Srr-2) found exclusively in RDP III-3 strains. The gene encoding Srr-2 was located within a putative accessory secretory locus that included secY2 and secA2 homologues and had a genetic organization similar to that of the secY2/A2 locus of staphylococci. In contrast, serotype III δ/ε-negative strains and strains representative of serotypes Ia, Ib, Ic and II shared a common Srr-encoding gene, srr-1, and an organization of the secY2/A2 locus similar to that of previously reported serotype Ic, δ/ε-negative serotype III and serotype V GBS strains. Representative serotype III δ/ε-positive strains had LD90 values 3–4 logs less than those of serotype III δ/ε-negative strains in a neonatal mouse model of infection. These results indicate that the RDP III-3/ST-17 lineage expresses Srr-2 and is highly virulent in an in vivo model of neonatal sepsis.

Phosphoglycerate kinase inhibits epithelial cell invasion by group B streptococci

2005 ◽  
Vol 38 (5-6) ◽  
pp. 189-200 ◽  
Author(s):  
Carey-Ann D. Burnham ◽  
Sandra E. Shokoples ◽  
Gregory J. Tyrrell
Keyword(s):  
Epithelial Cell ◽  
Cell Invasion ◽  
Phosphoglycerate Kinase ◽  
Group B Streptococci ◽  
Group B ◽  
Epithelial Cell Invasion

scholarly journals Characterization of a Novel Leucine-Rich Repeat Protein Antigen from Group B Streptococci That Elicits Protective Immunity

2005 ◽  
Vol 73 (3) ◽  
pp. 1671-1683 ◽  
Author(s):  
Ravin Seepersaud ◽  
Sean B. Hanniffy ◽  
Peter Mayne ◽  
Phil Sizer ◽  
Richard Le Page ◽  
...  
Keyword(s):  
Significant Risk ◽  
Invasive Disease ◽  
Invasive Infection ◽  
Dependent Manner ◽  
Leucine Rich Repeat ◽  
Group B Streptococci ◽  
Lethal Challenge ◽  
Life Threatening ◽  
Group B

ABSTRACT Group B streptococci (GBS) usually behave as commensal organisms that asymptomatically colonize the gastrointestinal and urogenital tracts of adults. However, GBS are also pathogens and the leading bacterial cause of life-threatening invasive disease in neonates. While the events leading to transmission and disease in neonates remain unclear, GBS carriage and level of colonization in the mother have been shown to be significant risk factors associated with invasive infection. Surface antigens represent ideal vaccine targets for eliciting antibodies that can act as opsonins and/or inhibit colonization and invasion. Using a genetic screen for exported proteins in GBS, we identified a gene, designated lrrG, that encodes a novel LPXTG anchored surface antigen containing leucine-rich repeat (LRR) motifs found in bacterial invasins and other members of the LRR protein family. Southern blotting showed that lrrG was present in all GBS strains tested, representing the nine serotypes, and revealed the presence of an lrrG homologue in Streptococcus pyogenes. Recombinant LrrG protein was shown in vitro to adhere to epithelial cells in a dose-dependent manner, suggesting that it may function as an adhesion factor in GBS. More importantly, immunization with recombinant LrrG elicited a strong immunoglobulin G response in CBA/ca mice and protected against lethal challenge with virulent GBS. The data presented in this report suggest that this conserved protein is a highly promising candidate antigen for use in a GBS vaccine.

scholarly journals Distribution of Pilus island and antibiotic resistance genes in Streptococcus agalactiae obtained from vagina of pregnant women in Yazd, Iran

2020 ◽  
Author(s):  
Mahdieh Nabavinia ◽  
Mohammad Bagher Khalili ◽  
Maryam Sadeh ◽  
Gilda Eslami ◽  
Mahmood Vakili ◽  
...  
Keyword(s):  
Antibiotic Resistance ◽  
Pregnant Women ◽  
Multiplex Pcr ◽  
Resistance Genes ◽  
Streptococcus Agalactiae ◽  
Antibiotic Resistance Genes ◽  
Invasive Disease ◽  
Group B Streptococci ◽  
Resistance Factors ◽  
Group B

Background and Objectives: Due to the important role of Streptococcus agalactiae, Group B streptococci (GBS), in production of invasive disease in neonates, investigation regarding the pathogenicity and antibiotic resistance factors is necessary in selecting the appropriate therapeutic agents. Beside capsule, the pilus has been currently recognized as an important factor in enhancing the pathogenicity of GBS. Resistance of GBS to selected antibiotics is noticeably increasing which is mainly due to the anomalous use of these drugs for treatment. The aim of this study was to determine the prevalence of pili genes followed by antibiotic susceptibility of GBS, previously serotyped, isolated from pregnant women in the city of Yazd, Iran. Materials and Methods: Fifty seven GBS from pregnant women were subjected to multiplex PCR for determination of PI-1, PI-2a and PI-2b pilus-islands and simultaneously, the phenotype of antibiotic resistance to penicillin, tetracycline, erythromycin, clindamycin, gentamycin and levofloxacin was determined. Antibiotic resistance genes (ermA, ermB, mefA, tetM, int-Tn) were further diagnosed using PCR and multiplex PCR. Results: PI-1+PI-2a with 71.9%; followed by PI-2a (21.1%) and PI-2b (7%) were observed. PI-1+PI-2a in serotype III was (73.2%), serotype II, Ia, Ib and V were 12.2%, 9.8%, 2.4% and 2.4% respectively. GBS penicillin sensitive was 89.5% and 96.5% resistance to tetracycline. The frequency of resistance genes were as follows: tetM (93%), ermA (33.3%), ermB (8.8%), int-Tn (80.7%) and mefA (0). Conclusion: Majority of GBS contained PI-1+PI-2a. Hence presence of this pilus stabilizes the colonization, therefore designing a program for diagnosing and treatment of infected pregnant women seems to be necessary.

scholarly journals In Vitro Repression of Brca1-associated RING Domain Gene, Bard1, Induces Phenotypic Changes in Mammary Epithelial Cells

1998 ◽  
Vol 143 (5) ◽  
pp. 1329-1339 ◽  
Author(s):  
Irmgard Irminger-Finger ◽  
Jesus V. Soriano ◽  
Geneviève Vaudan ◽  
Roberto Montesano ◽  
André-Pascal Sappino
Keyword(s):  
Epithelial Cell ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Ring Domain ◽  
Epithelial Cell Line ◽  
Missense Mutations ◽  
Collagen Gels ◽  
Normal Breast Epithelium ◽  
Phenotypic Changes

BRCA1-associated RING domain (BARD1) was identified as a protein interacting with the breast cancer gene product BRCA1. The identification of tumorigenic missense mutations within BRCA1 that impair the formation of BARD1–BRCA1 complexes, and of BARD1 mutations in breast carcinomas, sustain the view that BARD1 is involved in BRCA1-mediated tumor suppression. We have cloned the murine Bard1 gene and determined that its expression in different tissues correlates with the expression profile of Brca1. To investigate the function of Bard1, we have reduced Bard1 gene expression in TAC-2 cells, a murine mammary epithelial cell line that retains morphogenetic properties characteristic of normal breast epithelium. Partial repression of Bard1, achieved by the transfection of TAC-2 cells with plasmids constitutively expressing ribozymes or antisense RNAs, resulted in marked phenotypic changes, consisting of altered cell shape, increased cell size, high frequency of multinucleated cells, and aberrant cell cycle progression. Furthermore, Bard1-repressed cell clones overcame contact inhibition of cell proliferation when grown in monolayer cultures and lost the capacity to form luminal structures in three-dimensional collagen gels. These results demonstrate that Bard1 repression induces complex changes in mammary epithelial cell properties which are suggestive of a premalignant phenotype.

scholarly journals Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

2004 ◽  
Vol 72 (8) ◽  
pp. 4716-4722 ◽  
Author(s):  
Hiroshige Mikamo ◽  
Atul K. Johri ◽  
Lawrence C. Paoletti ◽  
Lawrence C. Madoff ◽  
Andrew B. Onderdonk
Keyword(s):  
Cytokine Production ◽  
Group B Streptococcus ◽  
A549 Cells ◽  
Interleukin 10 ◽  
Epithelial Cell Line ◽  
Group B Streptococci ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Group B

ABSTRACT The adherence to and invasion of the human epithelial cell line A549 by group B streptococcus (GBS) serotype VIII strains were compared with those of serotype III strains by a conventional method and the dynamic in vitro attachment and invasion system. Twenty GBS strains, including nine vaginal isolates and one invasive isolate each of serotypes III and VIII, were used in the conventional attachment and invasion assay. Adherence to and invasion of A549 cells by serotype VIII GBS strains were significantly greater (P < 0.0001) than those by serotype III strains for both the invasive strain and vaginal isolates. Cytokine production by A549 cells following stimulation with GBS serotypes III and VIII or their purified capsular polysaccharides (CPS) was measured. Serotype III strains stimulated significantly greater tumor necrosis factor alpha (TNF-α) (P < 0.0001) and interleukin-10 (IL-10) (P < 0.05) production than did serotype VIII strains. IL-8 production in response to serotype VIII was significantly higher (P < 0.001) than that in response to serotype III. TNF-α, IL-8, and IL-10 production was greater in A549 cells infected with GBS than in the untreated control cells. TNF-α production was significantly greater (P < 0.005) after stimulation with purified GBS serotype III CPS than after stimulation with serotype VIII CPS, a result similar to that after stimulation with whole GBS. IL-12 production by A549 cells was observed only in response to infection with GBS serotype III, resulting in the possibility of a greater TH1 response in serotype III GBS. These results suggest differences in immune responses to infection with GBS serotypes III and VIII.

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