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the class switching to IgA-antibody-producing precursor cells.22 The isotype class switching to IgA antibody is mediated by TGF-^, while switching to IgG1 and IgE antibodies is induced by IL-4.22 These cytokines may also be involved in the promotion of IgA antibody production and the inhibition of IgG1 and IgE antibody production by phycocyanin ingestion.

As shown in Figure 10.11A and other papers,23,29 serum OVA-specific IgE antibody, as well as IgG1, were not affected by 5-6 week treatment with phycocyanin. Further prolongation of phycocyanin treatment up to 8 weeks may contribute to the significant suppression of OVA-specific IgE antibody response, that is, suppression of Th2 function and/or enhancement of suppressor T cell or Th1 function. In contrast, significant reduction of intestinal vascular permeability in mice by Evans blue-leaking method was observed following 6-week treatment with phycocyanin (Figure 10.12). It was noted that the reduction of permeability preceded by 2 weeks the suppression of antigen-specific IgE level in the course of 8 weeks of phycocyanin ingestion. Remirez et al.37 reported that phycocyanin itself prevented allergic dermatitis in rats by inhibiting the release of histamine caused by compound 48/80. They also reported that oral administration of phycocyanin (50-200 mg/kg) 1 h before application of arachidonic acid prevented inflammatory edema in rat ears by reducing productions of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) through inhibiting the activity of cyclooxygenase (COX-2), a prostaglandin-synthesizing enzyme.38 Phycocyanin possibly alleviated the inflammation independent of IgE antibody. Spirulina products

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