Log in

Relevant bibliographies by topics / Group B streptococcus;human ureaplasmas / Journal articles

To see the other types of publications on this topic, follow the link: Group B streptococcus;human ureaplasmas.

Journal articles on the topic 'Group B streptococcus;human ureaplasmas'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Group B streptococcus;human ureaplasmas.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Estrada-Gutierrez, Guadalupe, Nardhy Gomez-Lopez, Veronica Zaga-Clavellina, Silvia Giono-Cerezo, Aurora Espejel-Nuñez, Marco Antonio Gonzalez-Jimenez, Salvador Espino y Sosa, David M. Olson, and Felipe Vadillo-Ortega. "Interaction between Pathogenic Bacteria and Intrauterine Leukocytes Triggers Alternative Molecular Signaling Cascades Leading to Labor in Women." Infection and Immunity 78, no. 11 (August 30, 2010): 4792–99. http://dx.doi.org/10.1128/iai.00522-10.

Full text

Abstract:

ABSTRACT Increased risk of preterm labor has been linked to cervicovaginal infection with Ureaplasma urealyticum and group B streptococci. Although various experimental models have been developed to study the role of amniochorion infection in preterm labor, they typically exclude the initial interaction between intrauterine leukocytes (recruited from decidual vessels into the avascular fetal membranes) and infecting bacteria. In this work, we ascertained whether inflammatory molecules secreted by bacterium-activated intrauterine leukocytes stimulate the amniochorion production of mediators involved in human labor. Using a two-step process beginning with placental circulating leukocytes as a proxy for intrauterine leukocytes, we found that coincubation of amniochorion explants with plasma from placental whole blood preincubated with group B streptococci resulted in a significant increase in tumor necrosis factor alpha (TNF-α) and matrix metalloproteinase 9 (MMP-9) levels in tissue. Extensive changes in the connective tissue arrangement and a decrease in collagen content demonstrated the degradation of the extracellular matrix following this treatment. In contrast, plasma from blood preconditioned with U. urealyticum induced a highly significant secretion of interleukin-1β (IL-1β) and prostaglandin E2 (PGE2) by the amniochorion without changes in the extracellular matrix organization or content. These data demonstrate that group B streptococci induce degradation of the amniochorion as a result of MMP-9 production, probably via TNF-α, whereas U. urealyticum stimulates the secretion of PGE2, probably via IL-1β, potentially stimulating myometrial contraction. Our study provides novel evidence that the immunological cells circulating within the uterine microenvironment respond differentially to an infectious agent, triggering alternative molecular signaling pathways leading to human labor.

APA, Harvard, Vancouver, ISO, and other styles

2

Pyrohova, V. I., S. O. Shurpyak, Yu R. Fayta, M. Y. Malachinska, and N. M. Kuz. "Comparative study of the efficacy of topical therapy of mixed vaginitis associated with cervicitis by combined medications." HEALTH OF WOMAN, no. 6(132) (July 30, 2018): 42–49. http://dx.doi.org/10.15574/hw.2018.132.42.

Full text

Abstract:

The objective: to increase the effectiveness of local therapy for recurrent nonspecific vaginitis associated with cervicitis in women of reproductive age on the basis of a comparative evaluation of combined drugs Terzhinan and Neo Penotran Forte. Materials and methods. A prospective, open comparative study included 56 women aged 27.5±2.8 years with recurrent nonspecific vaginitis and cervicitis who were randomized to the main group and comparison group. Patients of the main group (n=28) received the drug Terzhinan® (1 vaginal tablet in the evening, before bed, for 10 days). The comparison group included 28 patients who received Neo-Pentran Forte (1 vaginal suppository in the evening, before bedtime, for 10 days), one vaginal suppository containing 750 mg of metronidazole and 200 mg of miconazole nitrate. The complex clinical-paraclinical examination included the determination of the state of the vaginal microbiota using several methods in parallel: a bacterioscopy of vaginal smears stained by Gram, a bacteriological rapid method using AFGENITAL SYSTEM (Liofilchem®, Italy), real-time PCR (Florocenosis) with detection antigens of chlamydia, herpes simplex virus, human papillomavirus, trichomonads. Results. The main reason for the treatment of patients were abundant pathological discharge from the genital tract (73.2%), pruritus (37.5%) and burning (23.2%) in the vulva, pain during sexual intercourse (8.9%), while 33.9% of women expressed combined complaints. Attention was drawn to the significant frequency of dyshormonal pathology among women with recurrent cervico-vaginal infections. In the examined women, uterine leiomyoma was diagnosed (28.6%), genital endometriosis (19.6%), fibrocystic breast disease (37.5%), combined benign dyshormonal diseases of the genital organs (14.3%). About 21.4% of patients treatment of thyroid gland dysfunction (hypothyroidism). According to the comprehensive examination, in all patients of clinical groups, decompensated vaginal dysbiosis was diagnosed, which was manifested by a sharp decrease in the absence of Lactobacillus spp strains in 39.3% of patients and an increase in the number of isolated opportunistic and pathogenic microorganisms to 1011 CFU/ml with an increase in the number of microorganisms in microbial associations (from 2–3 to 5–6 conditionally pathogenic and pathogenic pathogens) in all the cases analyzed. When using the genital express system in vaginal contents, women of the main group identified Escherichia coli (17.9%), Pseudomonas spp. (10.7%), Gardnerella vaginalis (39.3%), Staphylococcus aureus (17 9%), Enterococcus faecalis (25.0%), Streptococcus Group B (10.7%), Candida spp. (46.4%), Mycoplasma spp./Ureaplasma ur. in the title > 105 (14.0%). In the comparison group, the spectrum of detected pathogenic and conditionally pathogenic microorganisms did not differ significantly from the data of the main group. 92.6% of patients in the main group had a pronounced positive clinical effect, and a positive microbiological effect was achieved in 96.4% of cases that persisted during the next two months of follow-up. Without additional prescription of antifungal agents, a positive effect was achieved in 84.6% of patients in the main group with mixed bacterial-candidiasis vaginitis at 54.5% in the comparison group. The independent recovery of the lactobacilli pool to a titer of 107–109 CFU/ml in 17.9% of patients with a lack of detection of lactobacilli before treatment. A similar effect was not observed in the comparison group. Сonclusion. In a comparative study of the results of the use of Terzhinan and Neo-Penotran Forte in monotherapy in patients with inflammatory diseases of the lower genitalia (nonspecific recurrent vaginitis and cervicitis), the high clinical and microbiological efficacy of Terzhinan has been demonstrated. Key words: mixed vaginitis, cervicitis, Terzhinan, Neo-Penotran Forte.

APA, Harvard, Vancouver, ISO, and other styles

3

Patras, Kathryn A., Philip A. Wescombe, Berenice Rösler, John D. Hale, John R. Tagg, and Kelly S. Doran. "Streptococcus salivarius K12 Limits Group B Streptococcus Vaginal Colonization." Infection and Immunity 83, no. 9 (June 15, 2015): 3438–44. http://dx.doi.org/10.1128/iai.00409-15.

Full text

Abstract:

Streptococcus agalactiae(group B streptococcus [GBS]) colonizes the rectovaginal tract in 20% to 30% of women and during pregnancy can be transmitted to the newborn, causing severe invasive disease. Current routine screening and antibiotic prophylaxis have fallen short of complete prevention of GBS transmission, and GBS remains a leading cause of neonatal infection. We have investigated the ability ofStreptococcus salivarius, a predominant member of the native human oral microbiota, to control GBS colonization. Comparison of the antibacterial activities of multipleS. salivariusstrains by use of a deferred-antagonism test showed thatS. salivariusstrain K12 exhibited the broadest spectrum of activity against GBS. K12 effectively inhibited all GBS strains tested, including disease-implicated isolates from newborns and colonizing isolates from the vaginal tract of pregnant women. Inhibition was dependent on the presence of megaplasmid pSsal-K12, which encodes the bacteriocins salivaricin A and salivaricin B; however, in coculture experiments, GBS growth was impeded by K12 independently of the megaplasmid. We also demonstrated that K12 adheres to and invades human vaginal epithelial cells at levels comparable to GBS. Inhibitory activity of K12 was examinedin vivousing a mouse model of GBS vaginal colonization. Mice colonized with GBS were treated vaginally with K12. K12 administration significantly reduced GBS vaginal colonization in comparison to nontreated controls, and this effect was partially dependent on the K12 megaplasmid. Our results suggest that K12 may have potential as a preventative therapy to control GBS vaginal colonization and thereby prevent its transmission to the neonate during pregnancy.

APA, Harvard, Vancouver, ISO, and other styles

4

Anthony, B. F., N. F. Concepcion, and K. F. Concepcion. "Human Antibody to the Group-Specific Polysaccharide of Group B Streptococcus." Journal of Infectious Diseases 151, no. 2 (February 1, 1985): 221–26. http://dx.doi.org/10.1093/infdis/151.2.221.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

Kasper, Dennis L., Michael R. Wessels, Hilde-Kari Guttormsen, Lawrence C. Paoletti, Morven S. Edwards, and Carol J. Baker. "Measurement of Human Antibodies to Type III Group B Streptococcus." Infection and Immunity 67, no. 8 (August 1999): 4303–5. http://dx.doi.org/10.1128/iai.67.8.4303-4305.1999.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Andreas, Nicholas J., Asmaa Al-Khalidi, Mustapha Jaiteh, Edward Clarke, Matthew J. Hyde, Neena Modi, Elaine Holmes, Beate Kampmann, and Kirsty Mehring Le Doare. "Role of human milk oligosaccharides in Group B Streptococcus colonisation." Clinical & Translational Immunology 5, no. 8 (August 26, 2016): e99. http://dx.doi.org/10.1038/cti.2016.43.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

MOYO, SYLVESTER R., JOHAN A. MAELAND, and KÅRE BERGH. "Typing of human isolates of Streptococcus agalactiae (group B streptococcus, GBS) strains from Zimbabwe." Journal of Medical Microbiology 51, no. 7 (July 1, 2002): 595–662. http://dx.doi.org/10.1099/0022-1317-51-7-595.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Tsai, Pei-Jane, Yee-Shin Lin, Chih-Feng Kuo, Huan-Yao Lei, and Jiunn-Jong Wu. "Group A Streptococcus Induces Apoptosis in Human Epithelial Cells." Infection and Immunity 67, no. 9 (September 1, 1999): 4334–39. http://dx.doi.org/10.1128/iai.67.9.4334-4339.1999.

Full text

Abstract:

ABSTRACT Internalization of group A streptococcus (GAS) by epithelial cells may have a role in causing invasive diseases. The purpose of this study was to examine the fate of GAS-infected epithelial cells. GAS has the ability to invade A-549 and HEp-2 cells. Both A-549 and HEp-2 cells were killed by infection with GAS. Epithelial cell death mediated by GAS was at least in part through apoptosis, as shown by changes in cellular morphology, DNA fragmentation laddering, and propidium iodide staining for hypodiploid cells. A total of 20% of A-549 cells and 11 to 13% of HEp-2 cells underwent apoptosis after 20 h of GAS infection, whereas only 1 to 2% of these cells exhibited spontaneous apoptosis. We further examined whether streptococcal pyrogenic exotoxin B (SPE B), a cysteine protease produced by GAS, was involved in the apoptosis of epithelial cells. The speB isogenic mutants had less ability to induce cell death than wild-type strains. When A-549 cells were cocultured with the mutant and SPE B for 2 h, the percentage of apoptotic cells did not increase although the number of intracellular bacteria increased to the level of wild-type strains. In addition, apoptosis was blocked by cytochalasin D treatment, which interfered with cytoskeleton function. The caspase inhibitors Z-VAD.FMK, Ac-YVAD.CMK, and Ac-DEVD.FMK inhibited GAS-induced apoptosis. These results demonstrate for the first time that GAS induces apoptosis of epithelial cells and internalization is required for apoptosis. The caspase pathway is involved in GAS-induced apoptosis, and the expression of SPE B in the cells enhances apoptosis.

APA, Harvard, Vancouver, ISO, and other styles

9

Liu, Yuxin, and Jinhui Liu. "Group B Streptococcus: Virulence Factors and Pathogenic Mechanism." Microorganisms 10, no. 12 (December 15, 2022): 2483. http://dx.doi.org/10.3390/microorganisms10122483.

Full text

Abstract:

Group B Streptococcus (GBS) or Streptococcus agalactiae is a major cause of neonatal mortality. When colonizing the lower genital tract of pregnant women, GBS may cause premature birth and stillbirth. If transmitted to the newborn, it may result in life-threatening illnesses, including sepsis, meningitis, and pneumonia. Moreover, through continuous evolution, GBS can use its original structure and unique factors to greatly improve its survival rate in the human body. This review discusses the key virulence factors that facilitate GBS invasion and colonization and their action mechanisms. A comprehensive understanding of the role of virulence factors in GBS infection is crucial to develop better treatment options and screen potential candidate molecules for the development of the vaccine.

APA, Harvard, Vancouver, ISO, and other styles

10

Lione, Viviane de Oliveira Freitas, Michelle Hanthequeste Bittencourt dos Santos, Jessica Silva Santos de Oliveira, Ana Luiza Mattos-Guaraldi, and Prescilla Emy Nagao. "Interferon-γ inhibits group B Streptococcus survival within human endothelial cells." Memórias do Instituto Oswaldo Cruz 109, no. 7 (November 2014): 940–43. http://dx.doi.org/10.1590/0074-0276140201.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Johri, Atul K., Joahnna Padilla, Gennady Malin, and Lawrence C. Paoletti. "Oxygen Regulates Invasiveness and Virulence of Group B Streptococcus." Infection and Immunity 71, no. 12 (December 2003): 6707–11. http://dx.doi.org/10.1128/iai.71.12.6707-6711.2003.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

12

Platt, Mark W., Norberto Correa Jr., and Carolyn Mold. "Growth of group B streptococci in human serum leads to increased cell surface sialic acid and decreased activation of the alternative complement pathway." Canadian Journal of Microbiology 40, no. 2 (February 1, 1994): 99–105. http://dx.doi.org/10.1139/m94-016.

Full text

Abstract:

Group B streptococcus type III is a major cause of neonatal death. The terminal sialic acid moiety of the group B streptococcus type specific capsule has been shown to be an important virulence factor. We demonstrate here that bacteria grown in human serum have increased cell surface sialic acid content compared with cells grown in common laboratory media. This sialic acid was removed by incubation with neuraminidase, showing that it was on the bacterial surface. Serum-dependent sialylation was dependent on metabolic activity, as the addition of chloramphenicol reduced the amount of added sialic acid by more than 90%. Probing the cell surface with an antibody specific for group B streptococcus type III capsular sialic acid showed an increase in antibody binding after growth in human serum. This effect could be lowered by incubating serum-grown cells in neuraminidase prior to antibody exposure. A group B streptococcus mutant that when grown in laboratory media lacks cell surface sialic acid showed significant cell surface sialic acid when grown in human serum. This increase was associated with a significantly decreased ability to bind C3 and hence activate the alternative complement pathway.Key words: group B streptococcus, capsule, human serum.

APA, Harvard, Vancouver, ISO, and other styles

13

Shakir, Salika M., Rahul Gill, Jonathan Salberg, E. Susan Slechta, Mark Feldman, Thomas Fritsche, Jill Clarridge, Susan E. Sharp, and Mark A. Fisher. "Clinical Laboratory Perspective on Streptococcus halichoeri, an Unusual Nonhemolytic, Lancefield Group B Streptococcus Causing Human Infections." Emerging Infectious Diseases 27, no. 5 (May 2021): 1309–16. http://dx.doi.org/10.3201/eid2705/203428.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Shakir, Salika M., Rahul Gill, Jonathan Salberg, E. Susan Slechta, Mark Feldman, Thomas Fritsche, Jill Clarridge, Susan E. Sharp, and Mark A. Fisher. "Clinical Laboratory Perspective on Streptococcus halichoeri, an Unusual Nonhemolytic, Lancefield Group B Streptococcus Causing Human Infections." Emerging Infectious Diseases 27, no. 5 (May 2021): 1309–16. http://dx.doi.org/10.3201/eid2705.203428.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Sitkiewicz, Izabela, Nicole M. Green, Nina Guo, Ann Marie Bongiovanni, Steven S. Witkin, and James M. Musser. "Transcriptome Adaptation of Group B Streptococcus to Growth in Human Amniotic Fluid." PLoS ONE 4, no. 7 (July 1, 2009): e6114. http://dx.doi.org/10.1371/journal.pone.0006114.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Alkuwaity, Khalil, Alexander Taylor, John E. Heckels, Kelly S. Doran, and Myron Christodoulides. "Group B Streptococcus Interactions with Human Meningeal Cells and Astrocytes In Vitro." PLoS ONE 7, no. 8 (August 10, 2012): e42660. http://dx.doi.org/10.1371/journal.pone.0042660.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Gray, B. M., D. G. Pritchard, J. D. Springfield, R. J. Benak, and H. C. Dillon. "Seroepidemiology of group B streptococcus type II antibody specificity." Epidemiology and Infection 101, no. 2 (October 1988): 347–54. http://dx.doi.org/10.1017/s0950268800054285.

Full text

Abstract:

SUMMARYThe specificity of human antibodies for the two major sidechain determinants of the type II group B streptococcal (GBS) polysaccharide was examined in 90 pairs of maternal and cord sera. Using an ELISA system, total antibody was measured against the complete (sialylated) type II antigen and the proportion of antibody against the galactose determinant was estimated by inhibition with free β–methylgalactopyranosided. Mothers colonized by type II or by other GBS types had higher levels of total specific antibody (means, 33 and 4–7 µg/ml, respectively) than those not colonized (mean, 2–2 µg/ml). Cord sera averaged 1–2 µg/ml lower than maternal sera. Colonization with GBS was also associated with higher levels against the galactose determinant (mean, 1.5&µg/ml, compared to 0–7µg/ml for those not colonized). The distribution of specificities favoured antibodies against the sialic acid determinant in maternal but not cord sera. Specificity as well as antibody level may play a role in the epidemiology of GBS type II.

APA, Harvard, Vancouver, ISO, and other styles

18

Vallejo, Jesus G., Douglas L. Mann, and Natarajan Sivasubramanian. "Group B Streptococcus Infection Activates Nuclear Factor Kappa B in Human Cord Blood Monocytes † 928." Pediatric Research 43 (April 1998): 160. http://dx.doi.org/10.1203/00006450-199804001-00949.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Jiang, Shengmei, and Michael R. Wessels. "BsaB, a Novel Adherence Factor of Group B Streptococcus." Infection and Immunity 82, no. 3 (December 16, 2013): 1007–16. http://dx.doi.org/10.1128/iai.01014-13.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

20

Zainudin, Zurina, Zainab Kassim, and Norlijah Othman. "Congenital Pneumonia." Journal of Pediatric Infectious Diseases 13, no. 04 (September 27, 2018): 255–67. http://dx.doi.org/10.1055/s-0038-1672131.

Full text

Abstract:

AbstractCongenital pneumonia is one of the common causes of respiratory distress at birth, with significant morbidity and mortality in neonates, especially among preterm infants, and particularly in developing countries. The etiological agents are many and vary between the developed and underdeveloped parts of the world. Group B streptococci have been attributed as the most common organisms causing severe pneumonia, particularly in developed countries. Human immunodeficiency virus (HIV) is now an increasing risk in underdeveloped countries such as Zimbabwe. Ureaplasma spp. have been highlighted as an important cause of congenital pneumonia in recent years. Clinical manifestations are often nonspecified, and majority of infections appear within the first 48 hours of life. Establishing the microbial diagnosis of congenital pneumonia is challenging. Molecular diagnosis using polymerase chain reaction has an extremely improved diagnostic yield as compared with other conventional detection methods. However, it is often associated with a high level of contamination and may not be available in most hospitals. Management of congenital pneumonia is multifaceted and the most vital is towards eliminating the possible incriminating agent. This review updates the current knowledge on congenital pneumonia and discusses its etiology, diagnosis, preventive strategies, and management.

APA, Harvard, Vancouver, ISO, and other styles

21

Silvestroni, Aurelio, Kelsea A. Jewell, Wan-Jung Lin, James E. Connelly, Melanie M. Ivancic, W. Andy Tao, and Lakshmi Rajagopal. "Identification of Serine/Threonine Kinase Substrates in the Human Pathogen Group B Streptococcus." Journal of Proteome Research 8, no. 5 (May 2009): 2563–74. http://dx.doi.org/10.1021/pr900069n.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Vornhagen, Jay, Phoenicia Quach, Verónica Santana-Ufret, Varchita Alishetti, Alyssa Brokaw, Blair Armistead, Hai Qing Tang, et al. "Human Cervical Mucus Plugs Exhibit Insufficiencies in Antimicrobial Activity Towards Group B Streptococcus." Journal of Infectious Diseases 217, no. 10 (February 7, 2018): 1626–36. http://dx.doi.org/10.1093/infdis/jiy076.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Whidbey, Christopher, Maria Isabel Harrell, Kellie Burnside, Lisa Ngo, Alexis K. Becraft, Lakshminarayan M. Iyer, L. Aravind, Jane Hitti, Kristina M. Adams Waldorf, and Lakshmi Rajagopal. "A hemolytic pigment of Group B Streptococcus allows bacterial penetration of human placenta." Journal of Experimental Medicine 210, no. 6 (May 27, 2013): 1265–81. http://dx.doi.org/10.1084/jem.20122753.

Full text

Abstract:

Microbial infection of the amniotic fluid is a significant cause of fetal injury, preterm birth, and newborn infections. Group B Streptococcus (GBS) is an important human bacterial pathogen associated with preterm birth, fetal injury, and neonatal mortality. Although GBS has been isolated from amniotic fluid of women in preterm labor, mechanisms of in utero infection remain unknown. Previous studies indicated that GBS are unable to invade human amniotic epithelial cells (hAECs), which represent the last barrier to the amniotic cavity and fetus. We show that GBS invades hAECs and strains lacking the hemolysin repressor CovR/S accelerate amniotic barrier failure and penetrate chorioamniotic membranes in a hemolysin-dependent manner. Clinical GBS isolates obtained from women in preterm labor are hyperhemolytic and some are associated with covR/S mutations. We demonstrate for the first time that hemolytic and cytolytic activity of GBS is due to the ornithine rhamnolipid pigment and not due to a pore-forming protein toxin. Our studies emphasize the importance of the hemolytic GBS pigment in ascending infection and fetal injury.

APA, Harvard, Vancouver, ISO, and other styles

24

Boyer, K. M., M. E. Klegerman, and S. P. Gotoff. "Development of IgM Antibody to Group B Streptococcus Type III in Human Infants." Journal of Infectious Diseases 165, no. 6 (June 1, 1992): 1049–55. http://dx.doi.org/10.1093/infdis/165.6.1049.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Boldenow, E., S. Jones, R. W. Lieberman, M. C. Chames, D. M. Aronoff, C. Xi, and R. Loch-Caruso. "Antimicrobial peptide response to Group B Streptococcus in human extraplacental membranes in culture." Placenta 34, no. 6 (June 2013): 480–85. http://dx.doi.org/10.1016/j.placenta.2013.02.010.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Hemming, V. G., K. Nagarajan, L. W. Hess, G. W. Fischer, S. R. Wilson, and L. S. Thomas. "Rapid in vitro Replication of Group B Streptococcus in Term Human Amniotic Fluid." Gynecologic and Obstetric Investigation 19, no. 3 (1985): 124–29. http://dx.doi.org/10.1159/000299021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Cieslewicz, Michael J., Donald Chaffin, Gustavo Glusman, Dennis Kasper, Anup Madan, Stephani Rodrigues, Jessica Fahey, Michael R. Wessels, and Craig E. Rubens. "Structural and Genetic Diversity of Group B Streptococcus Capsular Polysaccharides." Infection and Immunity 73, no. 5 (May 2005): 3096–103. http://dx.doi.org/10.1128/iai.73.5.3096-3103.2005.

Full text

Abstract:

ABSTRACT Group B Streptococcus (GBS) is an important pathogen of neonates, pregnant women, and immunocompromised individuals. GBS isolates associated with human infection produce one of nine antigenically distinct capsular polysaccharides which are thought to play a key role in virulence. A comparison of GBS polysaccharide structures of all nine known GBS serotypes together with the predicted amino acid sequences of the proteins that direct their synthesis suggests that the evolution of serotype-specific capsular polysaccharides has proceeded through en bloc replacement of individual glycosyltransferase genes with DNA sequences that encode enzymes with new linkage specificities. We found striking heterogeneity in amino acid sequences of synthetic enzymes with very similar functions, an observation that supports horizontal gene transfer rather than stepwise mutagenesis as a mechanism for capsule variation. Eight of the nine serotypes appear to be closely related both structurally and genetically, whereas serotype VIII is more distantly related. This similarity in polysaccharide structure strongly suggests that the evolutionary pressure toward antigenic variation exerted by acquired immunity is counterbalanced by a survival advantage conferred by conserved structural motifs of the GBS polysaccharides.

APA, Harvard, Vancouver, ISO, and other styles

28

SITKIEWICZ, IZABELA, and WALERIA HRYNIEWICZ. "Pyogenic Streptococci – Danger of Re-Emerging Pathogens." Polish Journal of Microbiology 59, no. 4 (2010): 219–26. http://dx.doi.org/10.33073/pjm-2010-034.

Full text

Abstract:

Beta-hemolytic, pyogenic streptococci are classified according to type of major surface antigen into A (Streptococcus pyogenes), B (Streptococcus agalactiae), C (multiple species including Streptococcus dysagalactiae) and G (multiple species including Streptococcus canis) Lancefield groups. Group A Streptococcus causes each year hundreds of thousands deaths globally as a result of infections and post-infectional sequelae. An increasing number of severe, invasive infections is caused by selected, specialized pathogenic clones. Within the last 50 years, an increasing number of human infections caused by groups B, C and G Streptococcus (GBS, GCS, GGS) has been observed worldwide. GBS was first identified as animal pathogen but the spectrum of diseases caused by GBS quickly shifted to human infections. Groups C and G Streptococcus are still regarded mostly as animal pathogens, however, an increased number of severe infections caused by these groups is observed. The increasing number of human infections caused worldwide by GCS/GGS can be a sign of similar development from animal to human pathogen as observed in case of GBS and this group will gain much more clinical interest in the future.The situation in Poland regarding invasive infections caused by pyogenic streptococci is underestimated.

APA, Harvard, Vancouver, ISO, and other styles

29

Keith, Mary Frances, Kathyayini Parlakoti Gopalakrishna, Venkata Hemanjani Bhavana, Gideon Hayden Hillebrand, Jordan Lynn Elder, Christina Joann Megli, Yoel Sadovsky, and Thomas Alexander Hooven. "Nitric Oxide Production and Effects in Group B Streptococcus Chorioamnionitis." Pathogens 11, no. 10 (September 28, 2022): 1115. http://dx.doi.org/10.3390/pathogens11101115.

Full text

Abstract:

Intrauterine infection, or chorioamnionitis, due to group B Streptococcus (GBS) is a common cause of miscarriage and preterm birth. To cause chorioamnionitis, GBS must bypass maternal-fetal innate immune defenses including nitric oxide (NO), a microbicidal gas produced by nitric oxide synthases (NOS). This study examined placental NO production and its role in host-pathogen interactions in GBS chorioamnionitis. In a murine model of ascending GBS chorioamnionitis, placental NOS isoform expression quantified by RT-qPCR revealed a four-fold expression increase in inducible NOS, no significant change in expression of endothelial NOS, and decreased expression of neuronal NOS. These NOS expression results were recapitulated ex vivo in freshly collected human placental samples that were co-incubated with GBS. Immunohistochemistry of wild type C57BL/6 murine placentas with GBS chorioamnionitis demonstrated diffuse inducible NOS expression with high-expression foci in the junctional zone and areas of abscess. Pregnancy outcomes between wild type and inducible NOS-deficient mice did not differ significantly although wild type dams had a trend toward more frequent preterm delivery. We also identified possible molecular mechanisms that GBS uses to survive in a NO-rich environment. In vitro exposure of GBS to NO resulted in dose-dependent growth inhibition that varied by serovar. RNA-seq on two GBS strains with distinct NO resistance phenotypes revealed that both GBS strains shared several detoxification pathways that were differentially expressed during NO exposure. These results demonstrate that the placental immune response to GBS chorioamnionitis includes induced NO production and indicate that GBS activates conserved stress pathways in response to NO exposure.

APA, Harvard, Vancouver, ISO, and other styles

30

Ma, Liping, Luo Xianming, Hongyu Li, Yiqing Li, Xie Shuangfen, and Wu Hui. "Group B Streptococcus Induce Platelet Activation Via Toll-Like Receptor 2." Blood 120, no. 21 (November 16, 2012): 1066. http://dx.doi.org/10.1182/blood.v120.21.1066.1066.

Full text

Abstract:

Abstract Abstract 1066 Objective: Group B Streptococcus (GBS), or Streptococcus agalactiae, is one of the most common cause of life-threatening sepsis in human newborns and immunosuppressed population. Patients suffering from sepsis often display low platelet counts characterized by thrombocytopenia as a result of platelet activation. Platelets, best known for their maintenance of hemostasis, have retained features of archetypal inflammatory cells corresponding to multiple roles in antimicrobial host defense. Nine members of the Toll-like receptors (TLRs) have been reported in human platelets, and TLRs in platelets play a fundamental role in both the initiation and propagation of the inflammatory response to microbial infection. We reported previously that LPS induces platelets activation and enhances platelets to release tumor necrosis factor-α by TLR 4. Since few confirm that platelets were activated by TLRs in directly binding to bacteria, the mechanism of activation of platelets in the interaction with pathogens remains unclear. Our research aimed to verify the hypothesis that the platelets selectively bind or adhere strains of GBS and aggregate, and to investigate the mechanism through which platelets become activated in sepsis upon binding to GBS and platelet TLR 2 involves in the process. Methods: Six strains of GBS were separated from septic patients. We determined GBS inducible platelet reactivity by using light transmission aggregometry, platelet bacterial adhesion assay, FCM and scanning electron microscopy. TLR2 expression was determined by RT-PCR and western blot assay. Results: After incubating platelets with strains of GBS separately, only three strains of GBS could induce platelets activation (platelets aggregation, adhesion and upgrated the expression of CD62P on platelet, Figure 1), meanwhile the activating ability and lag time were strain-dependent. Strains of GBS that were able to induce platelets activation also upregulated the expression of platelets TLR2 (in levels of RT-PCR and protein, Figure 2). However incubated with TLR 2 antibody, platelets no longer aggregated by the stimulation of GBS (Figure 3), suggesting TLR2 was involved in GBS induced platelets activation Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

31

Platt, M. "The effects of growth in human serum on an acapsular group B Streptococcus mutant." FEMS Immunology and Medical Microbiology 9, no. 3 (September 1994): 237–43. http://dx.doi.org/10.1016/0928-8244(94)90094-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

dos Santos, Michelle Hanthequeste Bittencourt, Andréia Ferreira Eduardo da Costa, Beatriz Jandre Ferreira, Simone Lima Souza, Pamella da Silva Lannes, Gabriela Silva Santos, Ana Luiza Mattos-Guaraldi, and Prescilla Emy Nagao. "A phosphoramidon-sensitive metalloprotease induces apoptosis of human endothelial cells by Group B Streptococcus." Antonie van Leeuwenhoek 104, no. 6 (September 20, 2013): 1125–33. http://dx.doi.org/10.1007/s10482-013-0034-y.

Full text

APA, Harvard, Vancouver, ISO, and other styles

33

Raff, H. V., P. J. Siscoe, E. A. Wolff, G. Maloney, and W. Shuford. "Human monoclonal antibodies to group B streptococcus. Reactivity and in vivo protection against multiple serotypes." Journal of Experimental Medicine 168, no. 3 (September 1, 1988): 905–17. http://dx.doi.org/10.1084/jem.168.3.905.

Full text

Abstract:

Group B streptococcal (GBS) infections cause significant mortality and morbidity among infants. Passive antibody immunotherapy has been proposed as treatment for infected infants. To this end, two human mAb-secreting cell lines were produced by EBV immortalization of human B cells. The mAbs were specific for the group B polysaccharide and bound to strains of all five serotypes as demonstrated by ELISA and crossed immunoelectrophoresis. The mAbs reacted and opsonized 100% (132/132) of the clinical isolates tested which represented all four capsule types. Both prophylactic and therapeutic protection with these mAbs were demonstrated in neonatal rats given lethal infections of types Ia and III human clinical isolates. These data indicate that a single human mAb directed against the group B carbohydrate can protect against GBS infections caused by the different serotypes. This antibody may be useful in the passive immunotherapy of infants infected with GBS.

APA, Harvard, Vancouver, ISO, and other styles

34

Budziaszek, Joanna, Magdalena Pilarczyk-Zurek, Izabela Sitkiewicz, and Joanna Koziel. "The corruption of innate immunity by Streptococcus anginosus group." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 16.21. http://dx.doi.org/10.4049/jimmunol.206.supp.16.21.

Full text

Abstract:

Abstract Streptococcus anginosus group (SAG), formerly known as Streptococcus milleri, consists of three distinct streptococcal species: Streptococcus anginosus, Streptococcus constellatus, and Streptococcus intermedius. SAG was considered as commensal bacteria of colon, oral cavity and vagina. Recent observation reported those bacteria as potent pathogens found in brain or liver abscess. Mechanism of SAG pathogenesis is still unknown, despite the strong set of clinical data. In our study, we determined the virulence of different SAG clinical isolates by examining the activity of hemolysins, DNAses and proteases. By using Dictyostelium discoideum as model for screening SAG virulence we selected a few high and low virulence strains out of 41 SAG isolates. Finally, we established and characterized the infection process of selected SAG strains by wax worm Galleria mellonella. Therefore, we aimed to characterize how those bacteria can interact with human innate immunity. In our experiments, using both human serum and whole blood we demonstrated, that these bacteria are resistant to killing by non-specific mechanisms of the immune response. Our studies have demonstrated that SAG have numerous virulence factors which differ among examined strains, and which allow bacteria to effectively colonize the human body and avoid elimination by the immune system. Supported by National Science Centre, Poland 2018/29/B/NZ6/00624

APA, Harvard, Vancouver, ISO, and other styles

35

Upadhyay, Kirtikumar, and Ajay Talati. "Neonatal Immune Responses during Group B Streptococcal Infections." Journal of Pediatric Infectious Diseases 12, no. 03 (June 7, 2017): 164–70. http://dx.doi.org/10.1055/s-0037-1603657.

Full text

Abstract:

AbstractGroup B streptococcus (GBS) still remains an important cause of neonatal sepsis in spite of various preventive strategies. The immune response of a neonate varies from an adult human immune system and makes a newborn more vulnerable to illness not typically manifested by adults. Microbial virulence, bacterial load, and immaturity of immune response system may explain the variation in severity of illness in term and preterm neonates. In this review, the mechanisms of GBS invasion and infection in a neonate are described. We also try to identify the host immune response to various bacterial components of GBS and possible future strategies to mitigate this immune response to improve neonatal outcomes after GBS sepsis.

APA, Harvard, Vancouver, ISO, and other styles

36

Campisi, Edmondo, Roberto Rosini, Maria Rosaria Romano, Evita Balducci, Vittoria Pinto, Barbara Brogioni, Riccardo De Ricco, et al. "Group B Streptococcus chimeric capsular polysaccharides as novel multivalent vaccine candidates." Glycoconjugate Journal 38, no. 4 (May 6, 2021): 447–57. http://dx.doi.org/10.1007/s10719-021-10000-4.

Full text

Abstract:

Abstract The capsular polysaccharide of the human pathogen Group B Streptococcus is a key virulence factor and vaccine candidate that induces protective antibodies when conjugated to carrier proteins. It consists of long polymeric chains of oligosaccharide repeating units, and each of the ten capsular serotypes described so far presents a unique chemical structure with distinct antigenic properties; therefore, broad protection against this pathogen could be achieved by a combination of ten glycoconjugates. Capsular polysaccharide biosynthesis and assembly follow a polymerase-dependent pathway that is widespread in encapsulated bacteria and is encoded by a polycistronic operon. Here we exploited the sequence similarity between the capsule operons of types V and IX to generate hybrid polysaccharides incorporating epitopes of both serotypes in a single molecule, by co-expressing their specific CpsM, O, I glycosyltransferases in a single isolate. Physicochemical and immunochemical methods confirmed that an engineered strain produced a high molecular weight chimeric polysaccharide, combining antigenic specificities of both type V and IX. By optimizing the copy number of key glycosyltransferase genes, we were able to modulate the ratio between type-specific epitopes. Finally, vaccination with chimeric glycoconjugates significantly decreased the incidence of disease in pups born from immunized mice challenged with either serotype. This study provides proof of concept for a new generation of glycoconjugate vaccines that combine the antigenic specificity of different polysaccharide variants in a single molecule, eliciting a protective immune response against multiple serotype variants.

APA, Harvard, Vancouver, ISO, and other styles

37

Mereghetti, Laurent, Izabela Sitkiewicz, Nicole M. Green, and James M. Musser. "Extensive Adaptive Changes Occur in the Transcriptome of Streptococcus agalactiae (Group B Streptococcus) in Response to Incubation with Human Blood." PLoS ONE 3, no. 9 (September 4, 2008): e3143. http://dx.doi.org/10.1371/journal.pone.0003143.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Larsson, Charlotte, Jan Holmgren, Gunnar Lindahl, and Charlotta Bergquist. "Intranasal Immunization of Mice with Group B Streptococcal Protein Rib and Cholera Toxin B Subunit Confers Protection against Lethal Infection." Infection and Immunity 72, no. 2 (February 2004): 1184–87. http://dx.doi.org/10.1128/iai.72.2.1184-1187.2004.

Full text

Abstract:

ABSTRACT Intranasal immunization of mice with Rib, a cell surface protein of group B streptococcus (GBS), conjugated to or simply coadministered with the recombinant cholera toxin B subunit, induces systemic immunoglobulin G (IgG) and local IgA antibody responses and confers protection against lethal GBS infection. These findings have implications for the development of a human GBS vaccine.

APA, Harvard, Vancouver, ISO, and other styles

39

Cunningham, M. W., J. M. McCormack, L. R. Talaber, J. B. Harley, E. M. Ayoub, R. S. Muneer, L. T. Chun, and D. V. Reddy. "Human monoclonal antibodies reactive with antigens of the group A Streptococcus and human heart." Journal of Immunology 141, no. 8 (October 15, 1988): 2760–66. http://dx.doi.org/10.4049/jimmunol.141.8.2760.

Full text

Abstract:

Abstract Human mAb were produced from tonsillar or PBL of normal individuals or patients infected with group A streptococci. Lymphocytes were purified on Ficoll-Hypaque gradients and stimulated in vitro with purified group A streptococcal membranes or M protein extracts. The mAb were selected for study based on their reaction with group A streptococci, pep M5 protein, and/or M6 Escherichia coli protein. Further analysis by Western immunoblot or competitive inhibition ELISA revealed that there were two types of antibodies: one type that reacted with myosin and DNA and the other type that reacted with myosin, keratin, and/or actin. The specificities of these human mAb are similar to specificities observed in our previous studies of murine mAb reactive with group A streptococci and heart Ag. For comparison, anti-myosin antibodies were affinity purified from the sera of infected or acute rheumatic fever patients and were shown to react with myosin and DNA as well as with group A streptococci and M protein. To affinity purify these antibodies from normal sera, five times the amount of sera was required to obtain detectable quantities. These data suggest that the human mAb reactive with group A streptococci and myosin reflect the antibodies seen in sera from infected patients or acute rheumatics and that the B lymphocyte clones capable of producing these cross-reactive antibodies are also present in normal individuals.

APA, Harvard, Vancouver, ISO, and other styles

40

Carlin, Aaron F., Yung-Chi Chang, Thomas Areschoug, Gunnar Lindahl, Nancy Hurtado-Ziola, Charles C. King, Ajit Varki, and Victor Nizet. "Group B Streptococcus suppression of phagocyte functions by protein-mediated engagement of human Siglec-5." Journal of Experimental Medicine 206, no. 8 (July 13, 2009): 1691–99. http://dx.doi.org/10.1084/jem.20090691.

Full text

Abstract:

Group B Streptococcus (GBS) is a leading cause of invasive bacterial infections in human newborns. A key GBS virulence factor is its capsular polysaccharide (CPS), displaying terminal sialic acid (Sia) residues which block deposition and activation of complement on the bacterial surface. We recently demonstrated that GBS Sia can bind human CD33-related Sia-recognizing immunoglobulin (Ig) superfamily lectins (hCD33rSiglecs), a family of inhibitory receptors expressed on the surface of leukocytes. We report the unexpected discovery that certain GBS strains may bind one such receptor, hSiglec-5, in a Sia-independent manner, via the cell wall–anchored β protein, resulting in recruitment of SHP protein tyrosine phosphatases. Using a panel of WT and mutant GBS strains together with Siglec-expressing cells and soluble Siglec-Fc chimeras, we show that GBS β protein binding to Siglec-5 functions to impair human leukocyte phagocytosis, oxidative burst, and extracellular trap production, promoting bacterial survival. We conclude that protein-mediated functional engagement of an inhibitory host lectin receptor promotes bacterial innate immune evasion.

APA, Harvard, Vancouver, ISO, and other styles

41

Kim, K. S., C. A. Wass, J. H. Kang, and B. F. Anthony. "Functional Activities of Various Preparations of Human Intravenous Immunoglobulin Against Type III Group B Streptococcus." Journal of Infectious Diseases 153, no. 6 (June 1, 1986): 1092–97. http://dx.doi.org/10.1093/infdis/153.6.1092.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Xia, Fan Di, Adeline Mallet, Elise Caliot, Cherry Gao, Patrick Trieu-Cuot, and Shaynoor Dramsi. "Capsular polysaccharide of Group B Streptococcus mediates biofilm formation in the presence of human plasma." Microbes and Infection 17, no. 1 (January 2015): 71–76. http://dx.doi.org/10.1016/j.micinf.2014.10.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Moncla, B. J., K. Pryke, and Charles E. Isaacs. "Killing of Neisseria gonorrhoeae, Streptococcus agalactiae (Group B Streptococcus), Haemophilus ducreyi, and Vaginal Lactobacillus by 3-O-Octyl-sn-Glycerol." Antimicrobial Agents and Chemotherapy 52, no. 4 (January 28, 2008): 1577–79. http://dx.doi.org/10.1128/aac.01023-07.

Full text

Abstract:

ABSTRACT The microbicide candidate octylglycerol inactivates sexually transmitted bacterial pathogens at concentrations which spare normal vaginal flora (lactobacillus). Standard minimum microbicidal concentration assays and time-kill assays revealed the drug concentrations and times required for inactivation. Octylglycerol concentrations must exceed the binding capacity of any human serum albumin to be effective.

APA, Harvard, Vancouver, ISO, and other styles

44

Hollasch, Heiko, Wolf-Dirk Niesen, and Jürgen Bardutzky. "Meningitis Caused by Streptococcus agalactiae after Professional Tooth Cleaning: First Case." Case Reports in Neurology 11, no. 1 (January 11, 2019): 1–3. http://dx.doi.org/10.1159/000495747.

Full text

Abstract:

We report the first case of meningitis caused by Streptococcus agalactiae (group B streptococcus; GBS) after professional tooth cleaning in a previously healthy patient. GBS is a common commensal of the human gastrointestinal and vaginal flora. Although occurrence in the oral flora is unusual, oral transmission and thus occurrence can be assumed.

APA, Harvard, Vancouver, ISO, and other styles

45

Jiang, Sheng-Mei, Nadeeza Ishmael, Julie Dunning Hotopp, Manuela Puliti, Luciana Tissi, Nikhil Kumar, Michael J. Cieslewicz, Hervé Tettelin, and Michael R. Wessels. "Variation in the Group B Streptococcus CsrRS Regulon and Effects on Pathogenicity." Journal of Bacteriology 190, no. 6 (January 18, 2008): 1956–65. http://dx.doi.org/10.1128/jb.01677-07.

Full text

Abstract:

ABSTRACT CsrRS (or CovRS) is a two-component regulatory system that controls expression of multiple virulence factors in the important human pathogen group B Streptococcus (GBS). We now report global gene expression studies in GBS strains 2603V/R and 515 and their isogenic csrR and csrS mutants. Together with data reported previously for strain NEM316, the results reveal a conserved 39-gene CsrRS regulon. In vitro phosphorylation-dependent binding of recombinant CsrR to promoter regions of both positively and negatively regulated genes suggests that direct binding of CsrR can mediate activation as well as repression of target gene expression. Distinct patterns of gene regulation in csrR versus csrS mutants in strain 2603V/R compared to 515 were associated with different hierarchies of relative virulence of wild-type, csrR, and csrS mutants in murine models of systemic infection and septic arthritis. We conclude that CsrRS regulates a core group of genes including important virulence factors in diverse strains of GBS but also displays marked variability in the repertoire of regulated genes and in the relative effects of CsrS signaling on CsrR-mediated gene regulation. Such variation is likely to play an important role in strain-specific adaptation of GBS to particular host environments and pathogenic potential in susceptible hosts.

APA, Harvard, Vancouver, ISO, and other styles

46

Goodrum, Kenneth J., and Jane Poulson-Dunlap. "Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells." Infection and Immunity 70, no. 1 (January 2002): 49–54. http://dx.doi.org/10.1128/iai.70.1.49-54.2002.

Full text

Abstract:

ABSTRACT Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis. Early-onset GBS pneumonia is characterized by marked pulmonary epithelial and endothelial cell injury. Innate proinflammatory responses to GBS infection that may contribute to the respiratory pathology include the synthesis and release of cytokines, prostaglandins, and nitric oxide (NO). The hypothesis that NO is directly induced in lung epithelial cells by invading GBS or indirectly induced by cytokines released by GBS-infected mononuclear cells was tested. A549 transformed human respiratory epithelial cells were directly cultured with GBS, cocultured with GBS-infected human mononuclear cells or purified macrophages, or exposed to conditioned culture medium from human mononuclear cells infected by GBS. The culture medium of A549 cultures was assayed for NO secretion, and the cell lysates were tested for presence of inducible nitric oxide synthase (iNOS) mRNA by reverse transcriptase PCR (RT-PCR). GBS-treated A549 cells neither secreted detectable NO nor expressed iNOS mRNA. GBS interaction with human mononuclear cells, however, stimulated release of soluble factors that readily induced iNOS mRNA expression and NO secretion by A549 cells. Inflammatory mediator-induced nitric oxide (NO) production by alveolar epithelium may exceed that of other lung cell types such as macrophages, and induction during GBS infection may play a significant role in pulmonary defense or free-radical-mediated lung injury.

APA, Harvard, Vancouver, ISO, and other styles

47

Johri, Atul K., Vilas Patwardhan, and Lawrence C. Paoletti. "Growth rate and oxygen regulate the interactions of group BStreptococcuswith polarized respiratory epithelial cells." Canadian Journal of Microbiology 51, no. 4 (April 1, 2005): 283–86. http://dx.doi.org/10.1139/w05-012.

Full text

Abstract:

We investigated growth conditions that regulate the ability of group B Streptococcus (GBS) to attach to, invade, and translocate through polarized human respiratory epithelial cells (RECs). GBS grown in a chemostat at a fast cell mass doubling time (td = 1.8 h), invaded RECs from both the apical and basolateral surfaces in higher numbers compared with those held at a td = 11 h. With the exception of adherence from the basolateral surface, GBS reached peak adherence to, invasion of, and translocation through RECs when held at the fast tdwith 15% dissolved oxygen compared with 0% dissolved oxygen. Growth rate and oxygen level strongly influence the interaction of GBS with polarized RECs and likely GBS pathogenicity.Key words: group B Streptococcus, oxygen, invasion, host–pathogen interactions, regulation, translocation.

APA, Harvard, Vancouver, ISO, and other styles

48

Granlund, Margareta, François Michel, and Mari Norgren. "Mutually Exclusive Distribution of IS1548 and GBSi1, an Active Group II Intron Identified in Human Isolates of Group B Streptococci." Journal of Bacteriology 183, no. 8 (April 15, 2001): 2560–69. http://dx.doi.org/10.1128/jb.183.8.2560-2569.2001.

Full text

Abstract:

ABSTRACT The present study shows that active, self-splicing group II intron GBSi1 is located downstream of the C5a-peptidase gene,scpB, in some group B streptococcus (GBS) isolates that lack insertion sequence IS1548. IS1548 was previously reported to be often present at the scpB locus in GBS isolated in association with endocarditis. Since none of 67 GBS isolates examined, 40 of which were of serotype III, harbored both IS1548 and GBSi1, these two elements are suggested to be markers for different genetic lineages in GBS serotype III. The DNA region downstream of scpB in GBS isolates harboring either GBSi1, IS1548, or none of these mobile elements was found to encode the laminin binding protein, Lmb, which shows sequence similarities to a family of streptococcal adhesins. IS1548 is inserted 9 bp upstream of the putative promoter for lmb, while the insertion site for GBSi1 is located 88 bp further upstream. Sequences highly similar to GBSi1 exist also in Streptococcus pneumoniae. An inverted repeat sequence, with features typical of transcription terminators, was identified immediately upstream of the insertion site for the group II intron both in the GBS and S. pneumoniae sequences. This motif is suggested to constitute a target for the GBS intron as well as for rather closely related introns in Bacillus halodurans, Pseudomonas alcaligenes, andPseudomonas putida. When transcripts containing the GBSi1 intron were incubated at high concentrations of ammonium and magnesium, a major product with the expected length and sequence for the ligated exons was generated. Unlike, however, all members of group II investigated so far, the excised intron was in linear, rather than in a branched (lariat), form.

APA, Harvard, Vancouver, ISO, and other styles

49

Lu, Jacky, Jamisha D. Francis, Miriam A. Guevara, Rebecca E. Moore, Schuyler A. Chambers, Ryan S. Doster, Alison J. Eastman, et al. "Antibacterial and Anti‐biofilm Activity of the Human Breast Milk Glycoprotein Lactoferrin against Group B Streptococcus." ChemBioChem 22, no. 12 (March 23, 2021): 2124–33. http://dx.doi.org/10.1002/cbic.202100016.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Park, Hae-Ryung, Sean M. Harris, Erica Boldenow, Richard C. McEachin, Maureen Sartor, Mark Chames, and Rita Loch-Caruso. "Group B streptococcus activates transcriptomic pathways related to premature birth in human extraplacental membranes in vitro†,‡." Biology of Reproduction 98, no. 3 (November 16, 2017): 396–407. http://dx.doi.org/10.1093/biolre/iox147.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!