Stimulating an immune response? Oral sex is associated with less endometritis.

Secondary analysis of the PID Evaluation and Clinical Health (PEACH) data suggests that among women presenting with signs and symptoms of pelvic inflammatory disease (PID), those who reported oral sex were less likely to have endometritis (adjusted odds ratio [OR] 0.5 [0.3-0.8]) than those who did not report oral sex. Adaptive immunity requires antigenic priming of the lymphatic system. As lymphatic tissue is abundant in the oropharynx, oral sex could lead to effective immune stimulation and prevent PID. To determine whether oral sex could be a protective factor for PID the relationship between self-reported oral sex and endometritis was analysed among 619 women with clinically suspected PID who participated in the PEACH study. Nearly one quarter of participants reported oral sex in the past four weeks. These women also reported a higher number of sexual partners, a new partner within the past four weeks and a higher frequency of sexual intercourse (all P < 0.03). They were more likely to smoke (P < 0.0001), drink alcohol (P < 0.004) and use recreational drugs (P < 0.02). Participants reporting oral sex were significantly less likely to be black or to have a positive test for Neisseria gonorrhoeae (7.8% versus 21.6%, P = 0.001). Women who disclosed oral sex were significantly less likely to have endometritis after adjusting for race, number of partners, recent new partner, smoking, alcohol use and drug use (adjusted OR 0.5 [0.3-0.8]). This is the first paper showing a negative association between oral sex and endometritis. This may be mediated by a protective immune response in the genital tract following priming in the oropharynx. This hypothesis needs to be tested in further studies.

T-cell regulation of polyclonal B-cell activation induced by extracts of oral bacteria associated with periodontal diseases.

These studies were designed to examine the role of regulatory T cells in the polyclonal antibody response of human peripheral blood lymphocytes to extracts of bacterial isolates commonly associated with periodontal disease. Polyclonal antibody responses to the organisms tested were found to be T cell dependent, as are most of the B-cell activators in the human system. Functional T helper activity was resistant to 1,500 rads of irradiation. Optimal polyclonal antibody responses to the bacterial extracts occurred at a 3:1 T-cell-to-B-cell ratio, whereas pokeweed mitogen-induced responses peaked at a 1:1 ratio, suggesting a difference in T-cell regulatory influences in response to these activators. Purified populations of T helper and suppressor cells exerted potent regulatory control of the responses to the bacterial extracts. These findings support the conclusion that regulatory T lymphocytes exert a potent modulating influence over the polyclonal response to periodontally associated bacteria and may play an important role in regulating the lymphocyte response in the diseased site.

Role of monocytes in polyclonal immunoglobulin production stimulated by sonicates of periodontally associated bacteria.

These studies were initiated to investigate monocyte regulation of polyclonal antibody responses of human peripheral blood lymphocytes stimulated by sonicates of periodontally associated bacteria. With pokeweed mitogen (PWM) as a positive reference, the role of monocytes in the peripheral blood lymphocyte response to Streptococcus sanguis and Wolinella HVS was examined by manipulating the number of monocytes and lymphocytes in culture. In comparison to PWM, optimal responses to the bacterial sonicates required very few monocytes (0.3% of the total cultured cells). Restoration of monocytes to physiological levels resulted in suppression of the response. PWM-stimulated responses were optimal at 5 to 15% monocyte content and were abolished after monocyte depletion. Individuals who were low responders or nonresponders to bacterial sonicates responded at normal levels after manipulation of monocyte concentration. Nonresponders produced normal levels of antibody when the monocyte concentration was reduced to 0.3% but were inhibited after monocyte reconstitution. The effects of monocyte concentration were tested over a wide dose range of bacterial sonicate and found to conform to the observed pattern throughout the dose range tested (10 to 1,000 micrograms/ml). The contrasting monocyte requirement of peripheral blood lymphocytes stimulated with PWM versus bacterial sonicates may reflect a quantitative difference in optimal macrophage concentration or may be due to a qualitative difference in lymphocyte-monocyte interactions in response to these activators.