the agglutination titres increased from the basal level of 1:56 before vaccination to 1:320 after finishing the primary immunization program, and it was still 1:140 one year later. Two weeks after the booster injection the mean titres were raised back to 1:343. Rüttgers quantified the total concentration of secretory IgA antibodies in the vaginal secretions of 192 women with bacterial vaginitis participating in a randomized, double-blind, placebo-controlled study. 95 patients were treated with SolcoTrichovac and 97 with placebo, according to the primary immunization scheme described above. The samples were tested using the enzyme‐linked immunosorbent assay according to Åkerlund et al. The mean baseline concentrations were similar in the two comparative groups. One month after the start of the therapy the sIgA concentration in the active-treatment group had risen significantly compared to the baseline and also in comparison to the placebo group. This difference gradually decreased over the subsequent months. After 12 months the sIgA concentration in the SolcoTrichovac group had fallen back to baseline value. About 35% of the actively treated patients had not developed a pronounced mucosal immune response. In these patients sIgA concentration of the vaginal secretion remained unchanged or showed only a short-lived elevation. Rüttgers observed that this group of patients by large overlapped with those, that had had reinfections during the follow-up period of 12 months, and concluded that vaginal sIgA concentration is a better correlate to immune protection than serum antibody titres. On the question of the mechanism underlying the induction of IgA-secreting plasma cells in the vaginal mucosa, Pavić and Stojković suggested that intramuscularly administered antigens may be transported to the local immunocompetent organ, in this case the vagina, and provoke a local secretory immune response. Patrolling dendritic cells exposed to killed bacterial antigens at a muscular injection site however typically do not migrate further than the local draining lymph nodes, where antigen presentation and the activation of T and B cells occur. Effector and memory lymphocytes in turn preferentially home back to the tissue where they were first activated, in this case the secondary lymph nodes. This is the reason why parenteral immunization with non-replicating antigens is generally considered ineffective in eliciting a mucosal immune response. Another possible explanation for an increased level of anti-aberrant-lactobacillus sIgA in vaginal secretions involves natural priming by mucosal infection at this site. Similarly to how subcutaneously administered killed whole-cell cholera vaccines reportedly only provoke substantial mucosal secretory