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Streptococcus suis is a major swine pathogen and important zoonotic agent causing mainly septicemia and meningitis. However, the mechanisms involved in host innate and adaptive immune responses toward S. suis as well as the mechanisms used by S. suis to subvert these responses are unknown. Here, and for the first time, the ability of S. suis to interact with bone marrow-derived swine dendritic cells (DCs) was evaluated. In addition, the role of S. suis capsular polysaccharide in modulation of DC functions was also assessed. Well encapsulated S. suis was relatively resistant to phagocytosis, but it increased the relative expression of Toll-like receptors 2 and 6 and triggered the release of several cytokines by DCs, including IL-1β, IL-6, IL-8, IL-12p40 and TNF-α. The capsular polysaccharide was shown to interfere with DC phagocytosis; however, once internalized, S. suis was readily destroyed by DCs independently of the presence of the capsular polysaccharide. Cell wall components were mainly responsible for DC activation, since the capsular polysaccharide-negative mutant induced higher cytokine levels than the wild-type strain. The capsular polysaccharide also interfered with the expression of the co-stimulatory molecules CD80/86 and MHC-II on DCs. To conclude, our results show for the first time that S. suis interacts with swine origin DCs and suggest that these cells might play a role in the development of host innate and adaptive immunity during an infection with S. suis serotype 2.

Streptococcus suis capsular type 2 is an important etiological agent of swine meningitis, and it is also a zoonotic agent. Since one hypothesis of the pathogenesis of S. suis infection is that bacteria enter the bloodstream and invade the meninges and other tissues in close association with mononuclear phagocytes, the objective of the present study was to evaluate the capacity of S. suis type 2 to adhere to macrophages. An enzyme-linked immunosorbent assay technique was standardized to simply and accurately measure the rate of bacterial attachment to phagocytic cells. Results were confirmed by plate counting. Adhesion was dependent on bacterial concentration and incubation time and was not affected by cytochalasin pretreatment of macrophages. Inhibition studies showed that the sialic acid moiety of the S. suis capsule would be, at least in part, responsible for bacterial recognition by macrophages. Serum preopsonization of bacteria increased adhesion levels. Complement would be partially implicated in the serum-enhanced binding of S. suis to cells. Adhesion varied among different S. suis type 2 isolates. However, high bacterial concentrations of several isolates were cytotoxic for cells, and these cytotoxic effects correlated with suilysin production. Indeed, hemolytic strain supernatants, as well as purified suilysin, reproduced cytotoxic effects observed with live bacteria, and these effects were inhibited by cholesterol pretreatment. Bacterial adhesion and cytotoxicity were confirmed by scanning and transmission electron microscopy. We hypothesize that attachment of bacteria to phagocytes could play an important role in the pathogenesis of S. suis infection by allowing bacterial dissemination and causing a bacteremia and/or septicemia. This interaction could also be related to the activation of the host inflammatory response observed during meningitis.

Streptococcus suis is one of the most important bacterial pathogens in weaned piglets and responsible for serious economic losses to the swine industry. Currently, mostly autogenous vaccines composed of killed bacteria (bacterins) are available. However, immunological and protective data from field studies are missing. We report for the first time a comparative field study on the immunological response induced by an autogenous vaccine applied to either piglets or sows in a farm with recurrent S. suis problems. (I) Piglets from non-vaccinated sows received an autogenous bacterin during the first week and at three weeks of age. (II) Sows received the vaccine at five and three weeks pre-farrowing and piglets were non-vaccinated. Levels, isotype profile and opsonophagocytosis capacity of the serum antibodies induced by vaccination were evaluated. Vaccination of piglets failed to induce an active immune response. Vaccination of sows induced a significant increase in anti-S. suis antibodies, mainly composed of IgG1. However, isotype switching was modulated by the S. suis serotype included in the vaccine formulation. Despite this antibody increase in vaccinated sows, transfer of maternal immunity to piglets was not different from the control group (i.e., piglets from non-vaccinated sows). Notably, levels of maternal antibodies in piglets were already very high with marked opsonophagocytosis capacity at one week of age, independently of the vaccination program. However, their levels decreased by three weeks of age, indicating possible absence of antibodies in the post-weaning high-risk period. These observations correlated with lack of clinical protection in the farm. Overall, a piglet or a sow vaccination program herein mostly failed to induce lasting protection in nursery piglets. An improvement of vaccine formulation or an optimized program may be required.

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