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Immunopotentiation of intraepithelial lymphocytes in the intestine by oral administrations of β-glucan

https://doi.org/10.1016/S0008-8749(03)00061-3Get rights and content

Abstract

Mice were orally administered with β-glucan, isolated from baker’s yeast, daily for one week (25 mg/day/mouse) and several immunoparameters in the digestive tract were examined. The most prominent change was an increase in the number of intraepithelial lymphocytes (IEL) in the intestine, although the number of lymphocytes in the liver remained unchanged. The absolute number of both αβT cells and γδT cells expressing CD8 antigens increased among IEL in the intestine. Primarily, liver lymphocytes showed a spontaneous production of Type 0 cytokine (simultaneous production of IFNγ and IL-4) while IEL did not produce any cytokines without stimulation. However, mice administered with β-glucan produced Type 1 cytokine, namely, production of IFNγ alone. These results suggest that β-glucan may be an important potentiator for mucosal immunity in the digestive tract.

Introduction

It is widely known that oats, mushrooms, and yeasts (including baker’s yeast and beer yeast) are good for the health because they stimulate intestinal movement [1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]. Thus, they can be used to ameliorate constipation and treat other bowel disorders. The major component of oats, mushrooms, and yeast is β-glucan, which is an undigestive sugar in humans. In light of these facts, it is speculated that β-glucan may also modulate mucosal immunity in the digestive tract. Thus, intestinal functions and the immune system are mutually regulated by parasympathetic nerves [13].

Cumulative evidence for mucosal immunity in the digestive tract has been raised during the past decade. Both the intestine [14], [15], [16] and the liver [17], [18] contain unique lymphocyte subsets of extrathymic origin. This is because the liver originated from the intestine in phylogeny as an excretion organ of bile [19]. However, the intestine and the liver developed in somewhat different ways as immune organs in subsequent phylogeny [20]. In this regard, we investigated how β-glucan differently modulates the immune system of the intestine and that of the liver. β-glucan was found to be an important potentiator for mucosal immunity in the intestine, but not in the liver.

Section snippets

Mice

C57BL/6 mice, maintained in the animal facility of Niigata University, were used in this study. All mice were fed under specific pathogen-free conditions.

Oral administration of β-glucan

β-glucan (Norwegian Beta 1, 3/1, 6 Glucan, Nakajima Suisan, Tokyo, Japan) was orally administered to mice (25 mg/day/mouse) for one week. Control mice were given PBS (pH 7.4).

Cell preparation

Hepatic lymphocytes were isolated by a previously described method [21]. Briefly, the liver was removed, pressed through 200-gauge stainless steel mesh, and suspended in

Increase in the number of IEL in the intestine by oral administration of β-glucan

Mice were orally administered with or without β-glucan for a week and the numbers of lymphocytes yielded by the intestine and liver were compared (Fig. 1). The number of IEL in the intestine was elevated up to fourfold by the administration of β-glucan in comparison with control mice. However, the number of lymphocytes in the liver remained unchanged by β-glucan.

In a preliminary study, we determined the dose of β-glucan in this study. Lower doses (e.g., 10 mg/day/mouse) of β-glucan than 25 

Discussion

In the present study, we demonstrated that β-glucan isolated from baker’s yeast increased the number and function of IEL in the intestine of mice when administered daily for a week. The number of lymphocytes yielded by the intestine increased more than fourfold in comparison with that of control mice. The most prominent change among IEL was seen in γδT cells expressing CD8 antigens. Spontaneous production of IFNγ (i.e., Type 1 cytokine profile) was also found in IEL of the intestine. These

Acknowledgments

This work was supported by a Grant-in-Aid for Scientific Research and Cancer Research from the Ministry of Education, Science, and Culture, Japan. We thank Mrs. Yuko Kaneko for preparation of the manuscript.

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