IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Spence, J. M.
Right arrow Articles by Clark, V. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Spence, J. M.
Right arrow Articles by Clark, V. L.

Infect. Immun., 09 1997, 3736-3742, Vol 65, No. 9
Copyright © 1997, American Society for Microbiology

A proposed role for the lutropin receptor in contact-inducible gonococcal invasion of Hec1B cells

JM Spence, JC Chen and VL Clark
Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, New York 14642, USA.

We previously reported the existence of a contact-inducible, enhanced invasion phenotype in the obligate human pathogen Neisseria gonorrhoeae. Our present studies showed that the ability of glutaraldehyde-fixed eucaryotic cells to convert gonococci (GC) to this invasive phenotype (Inv+) is limited to cells derived from reproductive tissues. We present evidence that GC recognize the lutropin receptor (LHr), which recognizes both luteinizing hormone and human chorionic gonadotropin (hCG), as the tissue-specific environmental signal that induces the conversion of GC to the Inv+ phenotype. By competitive binding studies, we showed that Inv+ GC bind to Hec1B cells, a human endometrial cell line, by a unique adhesin not present on noninduced GC and that this Inv+ GC-specific binding is completely blocked by the addition of hCG. We demonstrated that limiting the access of GC to LHr decreases the ability of the host cell to both convert GC to the Inv+ phenotype and serve as a target for Inv+ GC invasion. We propose a model of GC invasion of Hec1B cells in which the LHr plays a dual role both as an induction signal and as part of the internalization mechanism. This utilization of LHr could account for both the preponderance of complicated GC disease in women and the observed correlation of the disease with the onset of menses.


This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1997 by the American Society for Microbiology. All rights reserved.