title: The effect of orally administered glycogen on anti-tumor activity and natural killer cell activity in mice.
abstract: Natural killer (NK) cells, innate immune effectors that mediate rapid responses to various antigens, play an important role in potentiating host defenses through the clearance of tumor cells and virally infected cells. By using enzymatically synthesized glycogen (ESG) with the same characteristics as natural glycogen, we examined whether orally administered glycogen enhances the innate defense of tumor-implanted mice and the cytotoxicity of NK cells. Oral administration of ESG led to the suppression of tumor proliferation and the prolongation of survival times of tumor-bearing mice. Splenic NK activities of BALB/c mice treated orally with ESG were significantly higher than those of water-treated mice, which were used as a negative control. In addition, intraduodenal injections of ESG gradually and markedly lowered splenic sympathetic nerve activity, which has an inverse correlation with NK activity. Furthermore, ESG activated Peyer's patch cells to induce the production of macrophage inflammatory protein-2 (MIP-2), interleukin-6 (IL-6), and immunoglobulin A (IgA) from these cells. These results demonstrated that orally administrated glycogen significantly enhanced the cytotoxicity of NK cells by acting on Peyer's patch cells and autonomic nerves, and eventually induced the potentiation of host defenses. We propose that glycogen functions not only as an energy source for life support but also as an oral adjuvant for immunopotentiation.
authors.affiliation: Institute of Health Sciences, Ezaki Glico Co., Ltd., 4-6-5, Utajima, Nishiyodogawa-ku, Osaka 555-8502, Japan. kakutani-ryou@glico.co.jp
authors.forename: Ryo
authors.initials: R
authors.lastname: Kakutani
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Adachi
authors.forename: Hideki
authors.initials: H
authors.lastname: Kajiura
authors.forename: Hiroki
authors.initials: H
authors.lastname: Takata
authors.forename: Takashi
authors.initials: T
authors.lastname: Kuriki
authors.forename: Naohito
authors.initials: N
authors.lastname: Ohno
mesh_terms: D000276:Adjuvants, Immunologic / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D045744:Cell Line, Tumor; D054426:Chemokine CXCL2 / Q000276:immunology; D006003:Glycogen / Q000494:pharmacology / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000276:immunology; D007694:Killer Cells, Natural / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D009368:Neoplasm Transplantation; D009369:Neoplasms / Q000188:drug therapy* / Q000473:pathology; D010581:Peyer's Patches / Q000187:drug effects / Q000276:immunology; D051381:Rats; D013153:Splanchnic Nerves / Q000187:drug effects / Q000502:physiology; D013154:Spleen / Q000187:drug effects / Q000276:immunology / Q000294:innervation; D047368:Tumor Burden / Q000187:drug effects
chemical_list: D000276:Adjuvants, Immunologic; D000970:Antineoplastic Agents; D054426:Chemokine CXCL2; C404915:Cxcl2 protein, mouse; D015850:Interleukin-6; D006003:Glycogen