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Epidermal Growth Factor Receptor Signaling Enhances the Proinflammatory Effects of Staphylococcus aureus Gamma-Toxin on the Mucosa
Journal article   Open access   Peer reviewed

Epidermal Growth Factor Receptor Signaling Enhances the Proinflammatory Effects of Staphylococcus aureus Gamma-Toxin on the Mucosa

Aaron N Gillman, Laura M Breshears, Charles K Kistler, Patrick M Finnegan, Victor J Torres, Patrick M Schlievert and Marnie L Peterson
Toxins, Vol.9(7), p.202
06/28/2017
DOI: 10.3390/toxins9070202
PMCID: PMC5535149
PMID: 28657583
url
https://doi.org/10.3390/toxins9070202View
Published (Version of record) Open Access

Abstract

( ) produces many different exotoxins including the gamma-toxins, HlgAB and HlgCB. Gamma-toxins form pores in both leukocyte and erythrocyte membranes, resulting in cell lysis. The genes encoding gamma-toxins are present in most strains of and are commonly expressed in clinical isolates recovered from menstrual Toxic Shock Syndrome (mTSS) patients. This study set out to investigate the cytotoxic and proinflammatory effects of gamma-toxins on vaginal epithelial surfaces. We found that both HlgAB and HlgCB were cytotoxic to cultured human vaginal epithelial cells (HVECs) and induced cytokine production at sub-cytotoxic doses. Cytokine production induced by gamma-toxin treatment of HVECs was found to involve epidermal growth factor receptor (EGFR) signaling and mediated by shedding of EGFR ligands from the cell surface. The gamma-toxin subunits displayed differential binding to HVECs (HlgA 93%, HlgB 97% and HlgC 28%) with both components (HlgAB or HlgCB) required for maximum detectable binding and significant stimulation of cytokine production. In studies using full thickness ex vivo porcine vaginal mucosa, HlgAB or HlgCB stimulated a dose-dependent cytokine response, which was reduced significantly by inhibition of EGFR signaling. The effects of gamma-toxins on porcine vaginal tissue and cultured HVECs were validated using ex vivo human ectocervical tissue. Collectively, these studies have identified the EGFR-signaling pathway as a key component in gamma-toxin-induced proinflammatory changes at epithelial surfaces and highlight a potential therapeutic target to diminish toxigenic effects of infections.
Hemolysis - drug effects Inflammation - chemically induced Cervix Uteri - metabolism Epithelial Cells - metabolism Vagina - drug effects Epithelial Cells - drug effects Humans Bacterial Toxins - toxicity Inflammation - metabolism Receptor, Epidermal Growth Factor - metabolism Bacterial Proteins - toxicity Swine Hemolysin Proteins - toxicity Female Mucous Membrane - drug effects Vagina - cytology Cervix Uteri - drug effects Rabbits Cytokines - metabolism Erythrocytes - drug effects Mucous Membrane - metabolism Animals Signal Transduction - drug effects Receptor, Epidermal Growth Factor - antagonists & inhibitors Vagina - metabolism

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