Spence J M, Chen J C, Clark V L
Department of Microbiology and Immunology, School of Medicine and Dentistry, University of Rochester, New York 14642, USA.
Infect Immun. 1997 Sep;65(9):3736-42. doi: 10.1128/iai.65.9.3736-3742.1997.
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.
我们之前报道过，在人类专性病原体淋病奈瑟菌中存在一种接触诱导的、增强的侵袭表型。我们目前的研究表明，戊二醛固定的真核细胞将淋球菌（GC）转变为这种侵袭性表型（Inv+）的能力仅限于来自生殖组织的细胞。我们提供的证据表明，GC识别促黄体生成素受体（LHr），该受体可识别促黄体生成素和人绒毛膜促性腺激素（hCG），作为诱导GC转变为Inv+表型的组织特异性环境信号。通过竞争性结合研究，我们发现Inv+ GC通过一种非诱导GC所没有的独特黏附素与人类子宫内膜细胞系Hec1B细胞结合，并且添加hCG可完全阻断这种Inv+ GC特异性结合。我们证明，限制GC与LHr的接触会降低宿主细胞将GC转变为Inv+表型以及作为Inv+ GC侵袭靶点的能力。我们提出了一个GC侵袭Hec1B细胞的模型，其中LHr既作为诱导信号又作为内化机制的一部分发挥双重作用。LHr的这种利用可能解释了女性复杂GC疾病的优势以及该疾病与月经来潮的相关性。
