Study the Toll-like Receptor 2 and Dectin-1 in mice treated with beta‐ glucans and infected with Salmonella Typhimurium

Abstract

Objective: Toll-like receptors (TLRs) are essential components for the induction of innate immune responses
in different tissues including the small intestine, spleen and mesenteric lymph nodes. We investigated the
expression of TLR2 in these tissues in mice infected with Salmonella Typhimurium. In this study we have
examined how dectin-1, a lectin family receptor for β-glucans, collaborates with TLR-2 in recognition of
microbes.
Methods :In this study two groups of mice were treated with the β- glucan (local and commercial extract)
and infected with(1x10 6 CFU/ml) S. Typhimurium at different intervals group 1 at day zero and group 2
after seven days of the experiment .The immunohistochemistory assay has been performed to detect TLR-2
and dectine-1 in the tissues of small intestine, spleen and mesenteric lymph nodes of the mice; the principle of
this assay was done according to the manufacturer instructions (U.S.biological) .
Results: In the immunohistochemistory assay, positive cells were indicated by cytoplasmic staining and the
percentage of positive in 100 cells was recorded and graded. The grades were 1+ (<25%), 2+ (25-75%) and
3+ (>75%). Statistical analysis with Chi- Square tests revealed that there were significant differences (p˂0.05)
between groups, also between grades within the same group in the small intestine, spleen with TLR2
expression; also we demonstrated the same results with Dectin-1 expression in the small intestine and
mesenteric lymph nodes, except in the spleen which showed that there were no any relevant differences (p˂
0.05 ) between the groups and the cell- grades within the group itself.
Conclusions: The Oral treatment of both soluble β-glucan from Saccharomyces cerevisiae (Local and
commercial extracts) enhanced the host resistance in mice before the infection with S.Typhimurium. The
results of Immunohistochemical assay showed that the β- glucan also inducted the expression of Dectin-1 and
TLR-2 receptors on the cells, and also proved a collaborative reaction between these two receptors.