Gonorrhea is an exclusively human disease. Human host factors are known to be involved in supporting gonococcal infections leading to severe complications such as pelvic inflammatory disease (PID). It was suggested by other investigators that gonococcal cell (GC) attachment is mediated by specific ligands that selectively recognize receptors on certain types of human cells. The host factors important in attachment of GC are poorly understood.' It is critical to note that different mechanisms are probably operating in the attachment of gonococci to different kinds of cells. The mechanism operating in the attachment of GC to the fallopian tube seems to be species specific. The importance of host factors (TNF and CMP-NANA) as well as GC factors (protein 11, pili, and lipooligosaccharide) in infection of human tissues including fallopian tubes by GC was studied by many investigators?4 To the contrary, many unanswered questions exist concerning the mechanism of infection of the uterine endometrium by Neisseriu gonorrhoeue. The nature of the receptors and host factors that mediate specific interaction of GC with human endometrium is not completely understood. Recently, we described a new potential mechanism of GC attachment to human tissues in which complement C lq was a bridging molecule between GC and C lq receptors on human cells.'.* Glycoprotein C lq is a component of menstruum. Menstruum is known to be a predisposing host factor in developing upper genital tract infection. The fact that uterine and fallopian tube tissue is involved in PID raised the question of whether Clq is able to enhance attachment of GC to the uterus and fallopian tubes.
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