Group-B Streptococcal Infections

Gotoff, S P; Boyer, K M; Vogel, LawrenceC.; Kretschmer, R. R.

doi:10.1016/s0140-6736(79)90079-5

Cited by 7 publications

(6 citation statements)

References 8 publications

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“…At least one of 10 infants acquires GBS by vertical or horizontal transmission during the first month of life (1,2,28). The vast majority of these individuals have mucosal colonization without apparent illness.…”

Section: Discussionmentioning

confidence: 99%

“…Only 1% of the colonized neonates develop systemic GBS infection, indicating the presence of effective host defenses in most individuals. The elimination of invading GBS can be inferred to rest exclusively on the innate immune system, because protective levels of opsonizing Abs are rarely present in neonates (28). This same defense system may, however, mediate a lethal septic shock syndrome in response to overwhelming GBS challenge (3)(4)(5).…”

Section: Discussionmentioning

confidence: 99%

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Dual Role of TLR2 and Myeloid Differentiation Factor 88 in a Mouse Model of Invasive Group B Streptococcal Disease

Mancuso

Midiri

Beninati

et al. 2004

The Journal of Immunology

113

127

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Toll-like receptors (TLRs) are involved in pathogen recognition by the innate immune system. Different TLRs and the adaptor molecule myeloid differentiation factor 88 (MyD88) were previously shown to mediate in vitro cell activation induced by group B streptococcus (GBS). The present study examined the potential in vivo roles of TLR2 and MyD88 during infection with GBS. When pups were infected locally with a low bacterial dose, none of the TLR2- or MyD88-deficient mice, but all of the wild-type ones, were able to prevent systemic spread of GBS from the initial focus. Bacterial burden was higher in MyD88- than in TLR2-deficient mice, indicating a more profound defect of host defense in the former animals. In contrast, a high bacterial dose induced high level bacteremia in both mutant and wild-type mice. Under these conditions, however, TLR2 or MyD88 deficiency significantly protected mice from lethality, concomitantly with decreased circulating levels of TNF-α and IL-6. Administration of anti-TNF-α Abs to wild-type mice could mimic the effects of TLR2 or MyD88 deficiency and was detrimental in the low dose model, but protective in the high dose model. In conclusion, these data highlight a dual role of TLR2 and MyD88 in the host defense against GBS sepsis and strongly suggest TNF-α as the molecular mediator of bacterial clearance and septic shock.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Dual Role of TLR2 and Myeloid Differentiation Factor 88 in a Mouse Model of Invasive Group B Streptococcal Disease

Mancuso

Midiri

Beninati

et al. 2004

The Journal of Immunology

113

127

View full text Add to dashboard Cite

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“…Very different from Berry, and from each other, are the two stylistic commentaries of H. C. Gotoff (1979, which will be treated under 'Style' below. W. B. Tyrell's legal and historical commentary on Pro C. Rabirio (1978) takes the speech as a primary source for the legal and historical problems of the nature of the court and the political context that gives rise to the trial.…”

Section: CI the Speechesmentioning

confidence: 99%

Brill's Companion to Cicero

2002

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“…The GBS bacterium is a commensal organism in adults that colonizes the rectum and the urogenital and gastrointestinal tracts (13). To establish early onset disease, the bacterium must ascend from the acidic environment of the mother's vaginal mucosa to the lung epithelia of the neonate during birth and access the highly oxygenated environment of the blood (for a review, see reference 2).…”

mentioning

confidence: 99%

Abundance of the δ Subunit of RNA Polymerase Is Linked to the Virulence ofStreptococcus agalactiae

et al. 2006

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Group B streptococcus (GBS) remains a major cause of morbidity and mortality among newborn children. The bacterium is a commensal organism colonizing the rectum and the gastrointestinal and urogenital tracts of adults, but it can be transmitted to neonates by an ascending infection of the maternal genital tract or during parturition. We previously reported that a transposon insertion disrupting rpoE resulted in the decreased survival of the mutant in the neonatal rat sepsis model of GBS infection. rpoE encodes the ␦ protein, a subunit of RNA polymerase (RNAP) that has been characterized in Bacillus species. In this study, we confirm the association of the ␦ protein with purified GBS RNAP and show that it is expressed in strains representing all nine serotypes. Flow cytometric analysis of a reporter strain containing a transcriptional fusion of the rpoE promoter to gfp revealed that, in vitro, this gene is continuously expressed. Analysis of ␦ expression in the transposon mutant by quantitative Western blotting revealed a 10-fold reduction in relative abundance (which was linked to the attenuation in virulence that was observed for this mutant) compared to that for the wild-type strain. These data suggest that a minimum intracellular concentration of ␦ is necessary for this organism to cause disease.

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Group-B Streptococcal Infections

Cited by 7 publications

References 8 publications

Dual Role of TLR2 and Myeloid Differentiation Factor 88 in a Mouse Model of Invasive Group B Streptococcal Disease

Dual Role of TLR2 and Myeloid Differentiation Factor 88 in a Mouse Model of Invasive Group B Streptococcal Disease

Brill's Companion to Cicero

Abundance of the δ Subunit of RNA Polymerase Is Linked to the Virulence ofStreptococcus agalactiae

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