relationships between T. vaginalis and aberrant lactobacilli have not been studied. Nevertheless, multiple examples of gene transfer between the parasite and bacteria have been documented. Audrey de Koning argues that lateral transfer of the N-acetylneuraminate lyase gene from Pasteurellaceae to T. vaginalis may have been a key factor in the adaptation of Trichomonas to parasitism. In an analogous manner, Buret et al. suggest gene exchanges between enteropathogens and normal microbiota during acute enteric infection as one of the possible causative factors behind post-infectious intestinal inflammatory disorders. Alternative theory of the mechanism of action Goisis and his colleagues proposed an alternative hypothesis on the mechanism of action of SolcoTrichovac, suggesting that anti-lactobacillus antibodies may stimulate proliferation of lactobacilli rather than their (strain-specific) damage or inhibition. Among the circumstances they cited to support this theory, is their opinion that antibodies specific to one strain of Lactobacillus would most likely cross-react with several antigens present on various other strains (yet, both the concentration of anti-lactobacillus sIgA antibodies and lactobacillus counts have been demonstrated to increase in vaccinated women). Further they referred to the inconspicuous metabolic profile and the lack of a verified pathomechanism of the strains used in SolcoTrichovac, suggesting that they may represent mere morphotypes rather than pathogenic/unprotective biotypes. The proposed theory relies on analogies with other known examples of non-classical, stimulatory/homeostatic antibody-antigen interactions. Notably, the majority of intestinal bacterial cells in healthy individuals is bound by sIgA. The sIgA-coating of commensal enteric bacteria is believed to promote intestinal microbial homeostasis by a number of mechanisms. Secreted IgA anchors commensal bacteria to the mucus and facilitates biofilm formation, thereby limiting their translocation from the lumen into mucosal tissues. This minimizes activation of the innate immune system, a process termed "immune exclusion". Furthermore, the selective uptake of sIgA-microbe immune complexes by dendritic cells (DCs) in lymphoid follicles has been shown to induce semimaturation of the DCs. The resulting, so-called tolerogenic DCs downregulate the expression of T cell costimulatory molecules and proinflammatory cytokines. The altered immune signaling favours local processing of antigens and a rapid induction of low-affinitiy, broad-specificity IgA, leaving the systemic immune compartment ignorant about these organisms. In contrast, direct translocation of non-sIgA-coated microbes or microbial products across the epithelium preferentially results in proinflammatory signalling and a systemic response against the invading agent, involving affinity-matured serum antibodies of the classes IgA, IgE and IgG. Lastly, binding by sIgA can downregulate the expression