A PROPOSED ROLE FOR THE LUTROPIN RECEPTOR IN CONTACT-INDUCIBLE GONOCOCCAL INVASION OF HEC1B CELLS

We previously reported the existence of a contact-inducible, enhanced invasion phenotype in the obligate human pathogen Neisseria gonorrhoea e. 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 pr esent evidence that GC recognize the lutropin receptor (LHr), which re cognizes both luteinizing hormone and human chorionic gonadotropin (hC G), as the tissue-specific environmental signal that induces the conve rsion of GC to the Inv(+) phenotype, By competitive binding studies, w e 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 I nv(+) 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 an d serve as a target for Inv(+) GC invasion, We propose a model of GC i nvasion of Hec1B cells in which the LHr plays a dual role both as an i nduction signal and as part of the internalization mechanism, This uti lization of LHr could account for both the preponderance of complicate d GC disease in women and the observed correlation of the disease with the onset of menses.