Suppresses of Astragalus Polysaccharide on E. coli-Induced Injured Intestinal Microvascular through TLR4-NF-κB Signal Pathways in Chickens

Abstract

To investigate the hypothesis that APS can attenuate E. coli-induced microvascular dysfunction in chicken intestine, 60 0-day old male chickens were divided into three groups with 5 replications of 4 chicks. Chicken in the APS group were treated with 15 mg APS daily while the others were given 0 mg APS for 6 days. Then all 7-day old chicken were injected intraperitoneally by E. coli, except for the chicken in the control group. After 4 h, all chicken's intestinal samples were collected to detect gene expressions involved in inflammatory factors and adhesion molecules. Results showed that APS attenuated the signs of edema and hemorrhage in 7-day old chicken intestinal mucosa which were induced by E. coli injection. Consistently, APS significantly reduced the increasing mRNA levels of inflammatory factors such as Tumor necrosis factor-a (TNF-a), interleukin (IL)-1β and inducible nitric oxide synthase (iNOS) (p<0.05), the same results were observed in vascular adhesion molecules such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, we observed that APS supplementation in water suppressed significantly (p<0.05) the decline of reparative factors such as epithelial growth factor (EGF) and basic fibroblast growth factor (bFGF) in E. coli injected group. Furthermore, supplementation with APS substantially blocked (p<0.05) the increase in Toll-like receptor-4 (TLR4) and Nuclear factor (NF)-κB mRNA abundance (p=0.087) induced by E. coli infection. This study indicated that microvascular injured chicken intestine induced by E. coli would be attenuated with feeding APS, and the mechanism of repairing were probably mediated through TLR4-NF-κB signal pathways.

Bacillus Species as Direct-Fed Microbial Antibiotic Alternatives for Monogastric Production

“…DFM, such as those belonging to the genus Bacillus, can induce the expression of MUC2 gene responsible for mucin production, to neutralize the inflammation triggered by pathogenic germs [46]. When inducing an inflammatory response in chickens by intraperitoneal injection of lipopolysaccharide (LPS) from Escherichia coli [47], the group which was fed with the probiotic B. subtilis 1781 strain showed significant increase in the ileum MUC2 expression levels [48]. This up-regulation corroborated with remarkable reduce in inflammation signs as observed by decreased α-1-acid glycoprotein (α-1-AGP) expression, that is frequently associated with severe colitis [48].…”

Progress of Studies on Plant-Derived Polysaccharides Affecting Intestinal Barrier Function in Poultry

“…TLR4 receptor proteins bind to corresponding ligands to activate MAPK family proteins (JNK, p38 and extracellular signal-regulated kinase 1/2 (ERK1/2)), which ultimately activate NF-κB downstream signaling pathways to induce and promote the production of inflammatory cytokines such as TNF-α and IL-1β in the intestinal tract [ 69 ]. Furthermore, Su et al [ 27 ] showed that oral administration of 15 mg Astragalus polysaccharides to broilers significantly inhibited the gene expression of TLR4 and NF-κB in chickens challenged by Escherichia coli infection, inhibited intestinal microvascular injury induced by Escherichia coli through the regulatory pathway of TLR4-NF-κB, significantly decreased the mRNA levels of inflammatory factors TNF-α, IL-1β and inducible nitric oxide synthase (iNOS), decreased the gene expression levels of vascular adhesion molecule E-selectin, intercellular adhesion molecule-1 (ICAM1) and vascular cell adhesion molecule-1 (VCAM-1), and attenuated the mRNA expression of epithelial growth factor (EGF) and basic fibroblast growth factor (bFGF). It has also been reported that dietary Astragalus polysaccharides changed the immune microenvironment of jejunum mucosal epithelial cells and intestinal mucosal immune cells.…”