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ARS Home » Midwest Area » West Lafayette, Indiana » Livestock Behavior Research » Research » Publications at this Location » Publication #74683


item Eicher, Susan
item BLECHA, F

Submitted to: Meeting Abstract
Publication Type: Proceedings
Publication Acceptance Date: 11/11/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Previously, beta-glucan from SACCHROMYCES CEREVISIAE (0.05% of the diet) improved survival of mice challenged with STREPTOCOCCUS SUIS. Here we investigated effects of beta-glucan on relevant cellular molecule expression of induced peritoneal neutrophils and macrophages. Thirty mice per treatment were fed one of three beta-glucan treatments; none, 0.025%, or 0.05% of anticipated daily intake. After receiving beta-glucan for 28 days, neutrophils and macrophages were induced with thioglycolate. Type I and type II IL-1 receptors, CD18 (adhesion molecule), and CD32 (Fc receptor), were measured on neutrophils and macrophages. CD80 (activation molecule) was measured on macrophages. Double positive and double negative expression of neutrophil type I and II IL-1 receptors decreased with the 0.05% treatment compared to the 0.025% treatment and tended (P<.10) to decrease compared to the control. Neutrophil type I receptor tended (P=.08) to decrease with 0.05% compared to the 0.025% treatment. CD18 expression of neutrophils from 0.05% treated mice decreased compared to 0.025% treated mice, and tended (P=.12) to decrease from the controls. Neutrophil CD32 expression for the 0.025% treatment tended (P=.11) to increase compared with the control, and was numerically, but not significantly (P=.15) greater for the 0.05% treatment. Total number of macrophages tended (P=.13) to increase with 0.05% feeding. Macrophage IL-1 type II receptors increased with 0.025% treatment. Macrophage CD18 and CD32 did not differ among treatments, but CD80 tended (P=.11) to increase with 0.05% beta-glucan treatment. Regulation of immune response by 0.05% beta-glucan appears to include changes in expression of the IL-1 receptors on neutrophils and activation of macrophages.