The role of nontreponemal antibodies in the Treponema pallidum infection course is unclear. We investigated the effect of immunization with nontreponemal antigen on T. pallidum-challenged rabbits. Nontreponemal antigen was injected intravenously into rabbits in the nontreponemal group (n = 12) to elicit antibodies (≥1:64), and normal saline-injected rabbits were used as controls (n = 12). Then, rabbits were challenged with 10⁶ T. pallidum per site along their back. Lesion development was observed, and the injection sites were biopsied for mRNA analysis every week. Six rabbits from both groups were euthanized at 14 d and 28 d. The popliteal lymph nodes were extracted to assess infectivity using a rabbit infectivity test. The maximum lesion diameters were not different between the two groups (12.4 ± 0.9 mm in the nontreponemal group vs. 12.5 ± 1.0 mm in the control group, P = 0.386), but the time to maximum diameter appearance was delayed by approximately 4 d in the nontreponemal group (14.4 ± 1.6 d vs. 10.8 ± 1.9 d, P = 0.000). There were no significant differences in the proportions of lesions (58/60 (96.7%) vs. 59/60 (98.3%), P = 0.500) or ulcers (55/60 (91.7%) vs. 57/60 (95.0%), P = 0.359) between the two groups. An ulcer development delay of 5 d was observed in the nontreponemal group (19.3 ± 2.0 d vs. 14.0 ± 1.8 d, P = 0.000). IL-2 and IFN-γ mRNA expression in the nontreponemal group was significantly higher than that in the control group at 7 d and 14 d post-challenge. flaA mRNA expression and the rabbit infectivity test positive rate were not different between the two groups. Immunization with nontreponemal antigen altered the syphilis course in rabbits, resulting in delayed maximal lesion diameter and ulcer development, but it could not inhibit the spread of T. pallidum from primary lesion sites to viscera.

尚不清楚非梅毒螺旋体在梅毒螺旋体感染过程中的作用。我们研究了用非三链体抗原免疫接种的对梅毒螺旋体感染的兔子的影响。将非四链体抗原静脉注射到非三链体组（n = 12）的兔中，以引发抗体（≥1：64），并将注射生理盐水的兔子用作对照（n = 12）。然后，用10 ⁶ T. pallidum攻击兔子每个网站都沿着他们的背面。观察到病变的发展，并且每周对注射部位进行活检以进行mRNA分析。两组分别在14 d和28 d安乐死。提取in淋巴结，用兔子感染力测试评估感染力。两组之间的最大病变直径无差异（非三叉神经组为12.4±0.9 mm，对照组为12.5±1.0 mm，P  = 0.386），但最大直径出现时间延迟了约4 d。非戊二醛组（14.4±1.6 d vs. 10.8±1.9 d，P  = 0.000）。病变比例（58/60（96.7％）与59/60（98.3％），P  = 0.500）或溃疡（55/60（91.7％）与57/60（95.0％） ），P  = 0.359）。在非三叉神经组中观察到溃疡发展延迟为5天（19.3±2.0 d与14.0±1.8 d，P = 0.000）。攻击后7 d和14 d，非四联体组IL-2和IFN-γmRNA的表达明显高于对照组。两组之间的flaA mRNA表达和兔感染性试验阳性率无差异。非戊二醛抗原的免疫改变了家兔的梅毒病程，导致最大病灶直径的延迟和溃疡的发展，但不能抑制苍白锥虫从原发灶向内脏的扩散。