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Infection and Immunity, December 2004, p. 7005-7011, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7005-7011.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Immunostimulating Properties of Intragastrically Administered Acetobacter-Derived Soluble Branched (1,4)-ß-D-Glucans Decrease Murine Susceptibility to Listeria monocytogenes

Wei Li,¹ Toshiki Yajima,^1* Kimika Saito,¹ Hitoshi Nishimura,¹ Takashi Fushimi,² Yoshifumi Ohshima,² Yoshinori Tsukamoto,² and Yasunobu Yoshikai¹

Division of Host Defense, Research Center of Prevention of Infectious Disease, Medical Institute of Bioregulation, Kyushu University, Fukuoka,¹ Central Research Institute, Mitsukan Group Co., Ltd., Handa, Japan²

Received 27 April 2004/ Returned for modification 3 June 2004/ Accepted 27 August 2004

We previously found that AC-1, an extracellular polysaccharide, produced by Acetobacter xylinum and composed of (1,4)-ß-D-glucan with branches of glucosyl residues, showed a strong activity to induce production of interleukin-12 (IL-12) p40 and tumor necrosis factor alpha by macrophages in vitro via Toll-like receptor 4 (TLR-4) signaling. In the present study, we examined the effect of oral administration of AC-1 on protective immunity against Listeria monocytogenes. Mice were given AC-1 or phosphate-buffered saline (PBS) intragastrically 2 days before, on the day of, and 2 days after an intraperitoneal inoculation of L. monocytogenes. The survival rate of AC-1-treated mice was significantly improved and bacterial growth in AC-1-treated mice was severely retarded compared to those of PBS-treated mice after infection with L. monocytogenes. IL-12 p40 levels in serum and magnitudes of CD4⁺ Th1 and CD8⁺ Tc1 responses against Listeria antigen were significantly higher in AC-1-treated mice than in PBS-treated mice. The effect of AC-1 on antilisterial activity was diminished in C3H/HeJ mice carrying mutated TLR-4. Thus, AC-1, a potent IL-12 inducer through TLR-4, enhanced protective immunity against L. monocytogenes via augmentation of Th1 responses. These results suggest that infectious processes driven by intracellular microorganisms could be prevented to develop by the (1,4)-ß-D-glucan.

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* Corresponding author. Mailing address: Division of Host Defense, Research Center for Prevention of Infectious Diseases, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. Phone: 81-92-642-6962. Fax: 81-92-642-6973. E-mail: yajimato{at}bioreg.kyushu-u.ac.jp.

Editor: J. N. Weiser

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Infection and Immunity, December 2004, p. 7005-7011, Vol. 72, No. 12
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.12.7005-7011.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

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