Effect of human chorionic gonadotropin (hCG) on Neisseria gonorrhoeae invasion of and IgA secretion by human fallopian tube mucosa

Gary L. Gorby, Christopher M. Clemens, Lee R. Barley, Zell A. McGee

Research output: Contribution to journalArticle

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Abstract

The possible effect of human chorionic gonadotropin (hCG) on the mucosal immune response and susceptibility of the fallopian tube mucosa to invasion by Neisseria gonorrhoeae (gonococci) was investigated in the fallopian tube organ culture (FTOC) model. Immunohistochemical and radioreceptor assay techniques showed specific high affinity binding of hCG in vitro to the apices of non-ciliated fallopian tube cells (Kd approximately 10-9 m). Continuous exposure of the FTOC mucosa to hCG during infection with gonococci resulted in a marked increase (6- to 15-fold) in IgA secretion and significantly reduced gonococcal invasion (invasion score range 0.7 to 1.75) compared to infected control tissue which was not exposed to hCG (invasion score range 2.9 to 4.95, P ≤ 0.01). By contrast, exposure of the mucosa to hCG during the 24 h preceding gonococcal infection followed by the removal of hCG from the system at the time of infection resulted in enhanced gonococcal invasion (invasion score range 7.95 to 9.7, P <0.001). We conclude that hCG can modulate the mucosal immune response and susceptibility of fallopian tube epithelium to gonococcal invasion.

Original languageEnglish
Pages (from-to)373-384
Number of pages12
JournalMicrobial Pathogenesis
Volume10
Issue number5
DOIs
StatePublished - 1991

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Fallopian Tubes
Neisseria gonorrhoeae
Chorionic Gonadotropin
Immunoglobulin A
Mucous Membrane
Mucosal Immunity
Organ Culture Techniques
Infection
Radioligand Assay
Epithelium

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Infectious Diseases

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Effect of human chorionic gonadotropin (hCG) on Neisseria gonorrhoeae invasion of and IgA secretion by human fallopian tube mucosa. / Gorby, Gary L.; Clemens, Christopher M.; Barley, Lee R.; McGee, Zell A.

In: Microbial Pathogenesis, Vol. 10, No. 5, 1991, p. 373-384.

Research output: Contribution to journalArticle

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