Variations in attachment ofNeisseria gonorrhoeae to vaginal epithelial cells during the menstrual cycle and early pregnancy

1979 ◽  
Vol 167 (4) ◽  
pp. 231-238 ◽  
Author(s):  
Lars Forslin ◽  
Dan Danielsson ◽  
Viking Falk

1981 ◽  
Vol 32 (1) ◽  
pp. 194-197 ◽  
Author(s):  
J D Sobel ◽  
J Schneider ◽  
D Kaye ◽  
M E Levison


2018 ◽  
Author(s):  
Ying Wang ◽  
Raquel Ferrer-Espada ◽  
Yan Baglo ◽  
Xueping S. Goh ◽  
Kathryn D. Held ◽  
...  

ABSTRACTNeisseria gonorrhoeaeis the causative pathogen of the sexually transmitted disease gonorrhea, a disease at risk of becoming untreatable due to increasing antibiotic resistance. There is a critical need for the development of new anti-gonococcal therapies. In this study, we investigated the effectiveness of antimicrobial blue light (aBL), an innovative non-antibiotic approach, for the inactivation of antibiotic-resistantN.gonorrhoeae. Our findings indicated that aBL at 405 nm preferentially inactivated antibiotic-resistantN. gonorrhoeaeover the vaginal epithelial cells. Furthermore, no genotoxicity of aBL to the vaginal epithelial cells was observed at the exposure for inactivatingN. gonorrhoeae. aBL also effectively inactivatedN. gonorrhoeaethat had invaded into the vaginal epithelial cells. No gonococcal resistance to aBL developed after 15 successive cycles of sub-therapeutic inactivation. Endogenous aBL-active photosensitizing chromophores (porphyrins and flavins) inN. gonorrhoeaewere identified and quantified using ultra performance liquid chromatography, with coproporphyrin being the most abundant endogenous porphyrin species. Taken together, aBL at 405 nm represents a potent potential treatment for gonococcal infections.One Sentence SummaryaBL selectively inactivated antibiotic-resistantNeisseria gonorrhoeaenover normal vaginal epithelial cells.



1992 ◽  
Vol 144 (1) ◽  
pp. 36-38 ◽  
Author(s):  
C.R. Murphy ◽  
P.A.W. Rogers ◽  
M.J. Hosie ◽  
J. Leeton ◽  
L. Beaton


2021 ◽  
Vol 143 ◽  
pp. 103253
Author(s):  
Matthew William Woods ◽  
Muhammad Atif Zahoor ◽  
Jeffrey Lam ◽  
Puja Bagri ◽  
Haley Dupont ◽  
...  




2011 ◽  
Vol 92 (9) ◽  
pp. 1981-1993 ◽  
Author(s):  
Xiao-Dan Yao ◽  
Kenneth Lee Rosenthal

Viruses that establish persistent infections have evolved numerous strategies to evade host innate antiviral responses. We functionally assessed the role of herpes simplex virus type 2 (HSV-2) virion host shutoff (vhs) protein on innate immune sensing pathways in human vaginal epithelial cells (VK2 ECs). Infection of cells with wild-type (WT) HSV-2 significantly decreased expression of innate immune sensors of viral infection, Toll-like receptor (TLR)2, TLR3, retinoic acid inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (Mda-5), relative to cells infected with a mutant that lacks vhs (vhsB) or mock-infected cells. Transfection with HSV-2 vhs similarly decreased expression of TLR2, TLR3, RIG-I and Mda-5, which was also confirmed in human embryonic kidney (HEK) 293 cells. vhsB infection of VK2 cells caused robust increases in the active form of interferon regulatory factor (IRF)3 and its translocation to the nucleus compared with the WT. Additionally, IRF3 activation by Sendai virus and polyinosinic : polycytidylic acid-induced stimulation of beta interferon (IFN-β) was significantly inhibited in vhs-transfected cells. Overall, our findings provide the first evidence that HSV-2 vhs plays roles in selectively inhibiting TLR3 and RIG-I/Mda-5, as well as TLR2-mediated antiviral pathways for sensing dsRNA and effectively suppresses IFN-β antiviral responses in human vaginal ECs.



1998 ◽  
Vol 13 (4) ◽  
pp. 944-952 ◽  
Author(s):  
S. Yamada ◽  
H. Fujiwara ◽  
N. Kataoka ◽  
T. Honda ◽  
T. Nakayama ◽  
...  




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