Dectin1 activation of β-(1-3)/(1-6)-D-glucan produces an anti-mastitis effect in rats.Inflamm Res. 2011 Oct; 60(10):937-45.IR
A lipopolysaccharide (LPS)-induced mastitis model in rats was used to study the protective effect of β-glucan.
MATERIALS AND METHODS
On gestation day 10, β-glucan was administered to rats daily by gavage at either 0 (control), 0.1 mg/kg BW, 1 mg/kg BW and 10 mg/kg BW until parturition. LPS or pyrogen-free physiological saline was inoculated into the mammary gland 72 h after parturition and the rats were euthanized at 12 h post-infection.
LPS increased dectin1 and toll-like receptor 4 (TLR4) mRNA and protein expression significantly in mammary tissues. Tumor necrosis factor (TNF)-α, interleukin (IL)-1β, N-acetyl-β-D-glucosaminidase (NAGase), inducible nitric oxide synthase (iNOs) in mammary tissues and serum, and myeloperoxidase (MPO) in mammary tissues were significantly increased 12 h after LPS infusion. β-glucan administration could enhance dectin1 mRNA and protein expression while downregulating the expression of TLR4. Level of TNF-α, IL-1β in mammary tissues and serum, MPO, NAGase and iNOs activity in mammary tissues was decreased, but the level of IL-2 in serum was increased by β-glucan.
The results indicate that β-glucan may protect mammary tissue against LPS-induced rat acute mastitis.