The experimental immunomodulatory function of Spirulina was first reported in mice in 1994.8 This report introduced some evidence that Spirulina taken into mice facilitated antibody production, increased the ratio of activated peritoneal macrophages, and induced spleen cells to grow better in response to Con A.8 In spleen cells in culture, addition of the hot water extract of Spirulina leads to enhanced interleukin-1 (IL-1) and then antibody production.9 These results suggested that the initial target cells for Spirulina could be macrophages.
In 2002, human study on Spirulina was reported, where healthy male volunteers were given Spirulina orally every day for several weeks to be analyzed for the activity of their NK cells withdrawn at weekly or monthly intervals.4 The cells in the collected blood were incubated with IL-12 alone or together with IL-18 to observe the release of interferon (IFN)-gamma there in response to these cytokines. The NK activities, measured as the IFN-gamma production in response to IL-12/IL-18 and NK target killing activity, were much higher for the cells taken 2 months after the inset of the Spirulina administration than for the cells taken from the same volunteers before the administration. The results reflect the reported findings that NK reciprocally activates dendritic cells10 and IL-12/IL-18 may augment the NK cell activation.11
Successive studies suggested that Spirulina induces IFN-gamma and tumor cyto-toxicity in part dependent on NK activity. Spirulina appears to directly act on a certain lectin-like receptor on NK cells to induce NK-activating receptors,6 occurring independent of toll-like receptor (TLR). Unique points in this study are that (1) marked tumor regression is observed in mice with administration of Spirulina, suggesting that the NK cells actually participate in retardation of tumor growth, (2) Rae-1-positive tumor cells are selectively eliminated in Spirulina-fed mice, and (3) the S-form of NKG2D are induced in NK cells by Spirulina. Actually, PI3-kinase is activated secondary to the S-form of NKG2D and DAP10 in response to Spirulina extract in NK cells (Figure 9.1). It is also possible that unidentified pattern-recognition receptors (other than TLR) on dendritic cells participate in recognition of Spirulina extracts and make dendritic cells activate NK cells12 (Figure 9.2). These receptors are not TLRs but others that recognize pattern molecules in Spirulina.6 A major his-tocompatibility complex (MHC) low population of the tumor is selectively regressed by administration of Spirulina. Thus, the possible interpretation is that Spirulina extract activates mouse NK and the NK-mediated tumor cytotoxicity directs to the MHC-low population leading to retardation of tumor growth in the B16 syngeneic mouse model.
Structural investigation of Spirulina indicated that it contains glycolipids, such as O-fi-D-galactosyl-(1-1')-2',3/-di-O-acyl-D-glycerol, which possess fatty acid moieties, palmitic acid, and linoleic or linolenic acids.13 It is currently accepted that lipid moieties of microbes often serve as ligands of pattern-recognition receptors.14'15 Thus, it is not surprising that Spirulina glycolipids serve as ligands for pattern-recognition receptors. Inducing IFN-gamma supports this possibility since T cells as well as NK cells are main producers of IFN-gamma.4
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