The hormonal environment and estrogen receptor signaling alters infection .

Genital is the most common bacterial sexually transmitted infection in the United States and worldwide. Previous studies indicate that the progression of chlamydial infection is influenced by various factors, including the female sex hormones estrogen and progesterone. Sex hormone levels naturally fluctuate in women throughout their menstrual cycle.

Isolation, Physicochemical Characterization, Labeling, and Biological Evaluation of Mannans and Glucans.

The cell wall contains mannans and glucans that are recognized by the host immune system. In this chapter, we will describe the methods to isolate mannans and glucans from the C. albicans cell wall.

Lactate induces vascular permeability via disruption of VE-cadherin in endothelial cells during sepsis.

Circulating lactate levels are a critical biomarker for sepsis and are positively correlated with sepsis-associated mortality. We investigated whether lactate plays a biological role in causing endothelial barrier dysfunction in sepsis. We showed that lactate causes vascular permeability and worsens organ dysfunction in CLP sepsis.

The complexity of interactions between female sex hormones and infections.

Purpose Of Review: This review focuses specifically on the mechanisms by which female sex hormones, estrogen and progesterone, affect infections and .

Recent Findings: Recent data support previous work indicating that estrogen enhances chlamydial development via multiple mechanisms. Progesterone negatively impacts infections also through multiple mechanisms, particularly by altering the immune response.

Binding of Elementary Bodies by the Opportunistic Fungal Pathogen or Soluble β-Glucan, Laminarin, Inhibits Infectivity.

Microbial interactions represent an understudied facet of human health and disease. In this study, the interactions that occur between and the opportunistic fungal pathogen, were investigated. is a common component of the oral and vaginal microbiota responsible for thrush and vaginal yeast infections.

The type I interferon receptor is not required for protection in the Chlamydia muridarum and HSV-2 murine super-infection model.

Chlamydia trachomatis/HSV-2 vaginal co-infections are seen clinically, suggesting that these sexually transmitted pathogens may interact. We previously established an intravaginal Chlamydia muridarum/HSV-2 super-infection model and observed that chlamydial pre-infection protects mice from a subsequent lethal HSV-2 challenge. However, the mechanism of protection remains unknown.

Inhibition of Wnt Signaling Pathways Impairs Infection in Endometrial Epithelial Cells.

infections represent the predominant cause of bacterial sexually transmitted infections. As an obligate intracellular bacterium, is dependent on the host cell for survival, propagation, and transmission. Thus, factors that affect the host cell, including nutrition, cell cycle, and environmental signals, have the potential to impact chlamydial development.

Host Nectin-1 Promotes Chlamydial Infection in the Female Mouse Genital Tract, but Is Not Required for Infection in a Novel Male Murine Rectal Infection Model.

Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen, but more than 70% of patients fail to seek treatment due to the asymptomatic nature of these infections. Women suffer from numerous complications from chronic chlamydial infections, which include pelvic inflammatory disease and infertility. We previously demonstrated in culture that host cell nectin-1 knockdown significantly reduced chlamydial titers and inclusion size.

Zymosan-Induced Peritonitis: Effects on Cardiac Function, Temperature Regulation, Translocation of Bacteria, and Role of Dectin-1.

Zymosan-induced peritonitis is a model commonly used to study systemic inflammatory response syndrome and multiple organ dysfunction syndrome. However, effects of zymosan on cardiac function have not been reported. We evaluated cardiac responses to zymosan in mice and the role of β-glucan and dectin-1 in mediating these responses.

Chlamydial Pre-Infection Protects from Subsequent Herpes Simplex Virus-2 Challenge in a Murine Vaginal Super-Infection Model.

Chlamydia trachomatis and Herpes Simplex Virus-2 (HSV-2) genital tract co-infections have been reported in humans and studied in vitro but the clinical consequences are unknown. Limited epidemiologic evidence suggests that these co-infections could be more severe than single infections of either pathogen, but the host-pathogen interactions during co-infection remain uncharacterized. To determine whether disease progression and/or pathogen shedding differs between singly-infected and super-infected animals, we developed an in vivo super-infection model in which female BALB/c mice were vaginally infected with Chlamydia muridarum (Cm) followed later by HSV-2.

Progesterone antagonizes the positive influence of estrogen on Chlamydia trachomatis serovar E in an Ishikawa/SHT-290 co-culture model.

Studies indicate that estrogen enhances Chlamydia trachomatis serovar E infection in genital epithelial cells. Hormones have direct and indirect effects on endometrial epithelial cells. Estrogen and progesterone exposure induces endometrial stromal cells to release effectors that subsequently regulate growth and maturation of uterine epithelial cells.

Host nectin-1 is required for efficient Chlamydia trachomatis serovar E development.

Interaction of Herpes Simplex Virus (HSV) glycoprotein D (gD) with the host cell surface during Chlamydia trachomatis/HSV co-infection stimulates chlamydiae to become persistent. During viral entry, gD interacts with one of 4 host co-receptors: HVEM (herpes virus entry mediator), nectin-1, nectin-2 and 3-O-sulfated heparan sulfate. HVEM and nectin-1 are high-affinity entry receptors for both HSV-1 and HSV-2.

The multifaceted role of oestrogen in enhancing Chlamydia trachomatis infection in polarized human endometrial epithelial cells.

The oestrogen receptor (ER) α-β+ HEC-1B and the ERα+β+ Ishikawa (IK) cell lines were investigated to dissect the effects of oestrogen exposure on several parameters of Chlamydia trachomatis infection. Antibody blockage of ERα or ERβ alone or simultaneously significantly decreased C. trachomatis infectivity (45-68%).