OBJECTIVE: The purpose of this study was to evaluate transvaginal penetration of toxic shock syndrome toxin-1 and its effects on permeability and tissue integrity in vitro with the use of excised porcine vaginal mucosa. STUDY DESIGN: Permeability to tritiated water (1 and 10 microg/mL applied toxin) and transmucosal flux of (35)S-methionine-labeled toxic shock syndrome toxin-1 (10 and 20 microg/mL) for up to 12 hours were assessed with the use of a continuous flow perfusion system. The location of labeled toxin that penetrated the mucosal tissue strata was determined. The integrity of toxin-treated, intact, scalpel-incised tissue was evaluated histopathologically. RESULTS: Toxic shock syndrome toxin-1 caused a non-dose-dependent increase in mucosal permeability and traversed the intact mucosa at a low rate without disrupting tissue integrity. In incised vaginal mucosa, toxic shock syndrome toxin-1 induced subepithelial separation and atrophy that were analogous to clinically relevant vaginal lesions that were reported in fatal cases of menstrual toxic shock syndrome. CONCLUSION: An in vitro model could be used to demonstrate that toxic shock syndrome toxin-1 permeates the vaginal mucosa and distributes throughout the tissue. Histologic evaluation of tissues that were exposed to toxic shock syndrome toxin-1 demonstrated lesions that were similar to those lesions that were reported in cases of menstrual toxic shock syndrome.
OBJECTIVE: The purpose of this study was to evaluate transvaginal penetration of toxic shock syndrome toxin-1 and its effects on permeability and tissue integrity in vitro with the use of excised porcine vaginal mucosa. STUDY DESIGN: Permeability to tritiated water (1 and 10 microg/mL applied toxin) and transmucosal flux of (35)S-methionine-labeled toxic shock syndrome toxin-1 (10 and 20 microg/mL) for up to 12 hours were assessed with the use of a continuous flow perfusion system. The location of labeled toxin that penetrated the mucosal tissue strata was determined. The integrity of toxin-treated, intact, scalpel-incised tissue was evaluated histopathologically. RESULTS:Toxic shock syndrome toxin-1 caused a non-dose-dependent increase in mucosal permeability and traversed the intact mucosa at a low rate without disrupting tissue integrity. In incised vaginal mucosa, toxic shock syndrome toxin-1 induced subepithelial separation and atrophy that were analogous to clinically relevant vaginal lesions that were reported in fatal cases of menstrual toxic shock syndrome. CONCLUSION: An in vitro model could be used to demonstrate that toxic shock syndrome toxin-1 permeates the vaginal mucosa and distributes throughout the tissue. Histologic evaluation of tissues that were exposed to toxic shock syndrome toxin-1 demonstrated lesions that were similar to those lesions that were reported in cases of menstrual toxic shock syndrome.
Authors: Jeffrey Parsonnet; Melanie A Hansmann; Mary L Delaney; Paul A Modern; Andrea M Dubois; Wendy Wieland-Alter; Kimberly W Wissemann; John E Wild; Michaelle B Jones; Jon L Seymour; Andrew B Onderdonk Journal: J Clin Microbiol Date: 2005-09 Impact factor: 5.948
Authors: Marnie L Peterson; Kevin Ault; Mary J Kremer; Aloysius J Klingelhutz; Catherine C Davis; Christopher A Squier; Patrick M Schlievert Journal: Infect Immun Date: 2005-04 Impact factor: 3.441
Authors: Jeffrey Parsonnet; Melanie A Hansmann; Jon L Seymour; Mary L Delaney; Andrea M Dubois; Paul A Modern; Michaelle B Jones; John E Wild; Andrew B Onderdonk Journal: BMC Infect Dis Date: 2010-08-23 Impact factor: 3.090
Authors: Roderick A MacPhee; Wayne L Miller; Gregory B Gloor; John K McCormick; Jo-Anne Hammond; Jeremy P Burton; Gregor Reid Journal: Appl Environ Microbiol Date: 2013-01-11 Impact factor: 4.792
Authors: Amanda J Brosnahan; Mary J Mantz; Christopher A Squier; Marnie L Peterson; Patrick M Schlievert Journal: J Immunol Date: 2009-02-15 Impact factor: 5.422