Fibronectin-Binding Proteins Contribute to Colonization of the Female Reproductive Tract.

Methicillin-resistant Staphylococcus aureus (MRSA) is an opportunistic pathogen and frequent colonizer of human skin and mucosal membranes, including the vagina, with vaginal colonization reaching nearly 25% in some pregnant populations. MRSA vaginal colonization can lead to aerobic vaginitis (AV), and during pregnancy, bacterial ascension into the upper reproductive tract can lead to adverse birth outcomes. USA300, the most prominent MRSA lineage to colonize pregnant individuals, is a robust biofilm former and causative agent of invasive infections; however, little is known about how it colonizes and ascends in the female reproductive tract (FRT).

The Ubiquitous Human Skin Commensal Staphylococcus hominis Protects against Opportunistic Pathogens.

Staphylococcus hominis is frequently isolated from human skin, and we hypothesize that it may protect the cutaneous barrier from opportunistic pathogens. We determined that S. hominis makes six unique autoinducing peptide (AIP) signals that inhibit the major virulence factor accessory gene regulator () quorum sensing system of Staphylococcus aureus.

Role of MUC5B during Group B Streptococcal Vaginal Colonization.

The female reproductive tract (FRT) is a complex environment, rich in mucin glycoproteins that form a dense network on the surface of the underlying epithelia. Group B Streptococcus (GBS) asymptomatically colonizes 25-30% of healthy women, but during pregnancy can cause ascending infection or be transmitted to the newborn during birth to cause invasive disease. Though the cervicovaginal mucosa is a natural site for GBS colonization, the specific interactions between GBS and mucins remain unknown.

Human Milk Oligosaccharides versus Streptococcus: How a Human-Made Natural Product Protects Us from Pathogens.

Group B Streptococcus (GBS) is a Gram-positive bacterium that colonizes the lower gastrointestinal tract, and in females, the urogenital tract, in up to 30% of healthy adults. However, GBS is a leading cause of mortality and morbidity in newborns due to ascending infection of the womb or by neonatal acquisition during vaginal passage. GBS neonatal disease manifests as pneumonia, sepsis, or meningitis, and an estimated 4 million newborns die each year globally.

Genetic screen for suppressors of increased silencing in rpd3 mutants in Saccharomyces cerevisiae identifies a potential role for H3K4 methylation.

Several studies have identified the paradoxical phenotype of increased heterochromatic gene silencing at specific loci that results from deletion or mutation of the histone deacetylase (HDAC) gene RPD3. To further understand this phenomenon, we conducted a genetic screen for suppressors of this extended silencing phenotype at the HMR locus in Saccharomyces cerevisiae. Most of the mutations that suppressed extended HMR silencing in rpd3 mutants without completely abolishing silencing were identified in the histone H3 lysine 4 methylation (H3K4me) pathway, specifically in SET1, BRE1, and BRE2.