Modulation of the type I hypersensitivity late phase reaction to OVA by Propionibacterium acnes-soluble polysaccharide.

Late phase reaction (LPR) of immediate hypersensitivity is a Th2 response characterized by eosinophil recruitment and related to allergic asthma pathogenesis. Several strategies were developed trying to control the tissue damage observed in this reaction. Recently, we verified that killed Propionibacterium acnes (P. acnes), a Gram-positive bacillus, immunomodulated LPR in a murine model, potentiating or suppressing it depending on the treatment protocol used. However, the bacterium compounds responsible for this effect are not known, leading us to investigate if P. acnes purified soluble polysaccharide (PS) could be a major component involved on the modulation induced by the bacterium. Recently, we demonstrated that PS, like P. acnes, induces adjuvant effect on DNA vaccine, increases bone marrow dendritic cell precursors in vivo and its maturation in vitro, and modulates in vitro macrophage tumoricidal activity. Herein, we determined the chemical PS composition, which is mainly constituted by galactopyranose, ribopyranose, arabinopyranose, glucopyranose, ribofuranose and mannopyranose, and analyzed its capacity to modulate the immediate hypersensitivity in mice. Animals were subcutaneously implanted with coagulated hen's egg white (HEW) and 14 days later challenged with ovalbumin (OVA) in the footpad, developing a typical LPR after 24h. Similarly to the whole bacterium, Th2 response to OVA was potentiated when PS was administered concomitantly to HEW implantation, by increase in footpad eosinophilia and IL-4-producing spleen cells, and decrease in anti-OVA IgG2a titers and IL-12- or IFN-gamma-producing cells. On the other hand, the reaction was abrogated when HEW implantation was performed 1 week after PS-treatment, by decrease in footpad swelling, eosinophilia and anti-OVA IgG1 levels, and increase in IgG2a titers and IL-12-producing cells. These data suggest that PS seems to be the major P. acnes compound responsible for its effects on the modulation of immediate hypersensitivity reaction in mice.