Background:Escherichia coli(E.coli)infection in humans and animals usually comes with gut dysbiosis,which is potential culprit to skeletal health,it is still unclear to whether diet interfered gut microbiome changes c...Background:Escherichia coli(E.coli)infection in humans and animals usually comes with gut dysbiosis,which is potential culprit to skeletal health,it is still unclear to whether diet interfered gut microbiome changes can be a protective strategy to bone loss development.Here,the effects of resistant starch from raw potato starch(RPS),a type of prebiotic,on E.coli-induced bone loss and gut microbial composition in meat ducks were evaluated.Results:The results showed that dietary 12%RPS treatment improved bone quality,depressed bone resorption,and attenuated the pro-inflammatory reaction in both ileum and bone marrow.Meanwhile,the 12%RPS diet also increased the abundance of Firmicutes in E.coli-treated birds,along with higher production of short-chain fatty acids(SCFAs)especially propionate and butyrate.Whereas addition ofβ-acid,an inhibitor of bacterial SCFAs production,to the drinking water of ducks fed 12%RPS diet significantly decreased SCFAs level in cecum content and eliminated RPS-induced tibial mass improvement.Further,treatment with MI-2 to abrogate mucosa-associated lymphoid tissue lymphoma translocation protein 1(Malt1)activity replicated the protective role of dietary 12%RPS in E.coli-induced bone loss including reduced the inhibition on nuclear factorκB(NF-κB)inflammasome activation,decreased bone resorption,and improved bone quality,which were correlated with comparable and higher regulatory T cells(Treg)frequency in MI-2 and 12%RPS group,respectively.Conclusions:These findings suggested that the diet with 12%RPS could alleviate E.coli-induced bone loss in meat ducks by changing the gut microbial composition and promoting concomitant SCFAs production,and consequently inhibiting Malt1/NF-κB inflammasome activation and Treg cells expansion.展开更多
Background:Consumption of resistant starch(RS)has been associated with various intestinal and systemic health benefits,but knowledge of its effects on intestinal health and inflammatory response in stressed birds is l...Background:Consumption of resistant starch(RS)has been associated with various intestinal and systemic health benefits,but knowledge of its effects on intestinal health and inflammatory response in stressed birds is limited.Here,we examined how dietary RS supplementation from 12%raw potato starch(RPS)modulated inflammatory severity induced by lipopolysaccharide(LPS)in meat ducks.Results:LPS administration at 14,16,and 18 d(chronic challenge)decreased body weight(BW)and glucagon-like peptide 1 receptor(GLP-1R)level with higher intestinal permeability and inflammation,evident by higher proinflammatory cytokine levels.Dietary 12%RPS supplementation enhanced Claudin-1 and GLP-1R expression,along with lower levels of inflammatory factors in both ileum and serum.Microbiome analysis showed that RS treatment shifted microbial structure reflected by enriched the proportion of Firmicutes,Bifidobacterium,Ruminococcus,etc.Dietary RS addition also significantly increased the concentrations of propionate and butyrate during chronic LPS challenge.Furthermore,response to acute challenge,the ducks received 2 mg/kg BW LPS at 14 d had higher concentrations of serum endotoxins and inflammatory cytokines,as well as upregulated transcription of toll like receptor 4(TLR4)in ileum when compared to control birds.Analogous to GLP-1 agonist liraglutide,dietary RS addition decreased endotoxins and inflammation cytokines,whereas it upregulated the GLP-1 synthesis related genes expression.Meanwhile,dietary RS supplementation suppressed the acute LPS challenge-induced TLR4 transcription.Conclusions:These data suggest that dietary 12%RPS supplementation could attenuate the LPS-induced inflammation as well as intestinal injury of meat ducks,which might involve in the alteration in gut microbiota,SCFAs production and the signaling pathways of TLR4 and GLP-1/GLP-1R.展开更多
基金the National Natural Science Foundation of China(No.31772622)National Natural Science Foundation of China(No.32072748)Doctoral Fellowship from Henan Agricultural University(No.0501182)。
文摘Background:Escherichia coli(E.coli)infection in humans and animals usually comes with gut dysbiosis,which is potential culprit to skeletal health,it is still unclear to whether diet interfered gut microbiome changes can be a protective strategy to bone loss development.Here,the effects of resistant starch from raw potato starch(RPS),a type of prebiotic,on E.coli-induced bone loss and gut microbial composition in meat ducks were evaluated.Results:The results showed that dietary 12%RPS treatment improved bone quality,depressed bone resorption,and attenuated the pro-inflammatory reaction in both ileum and bone marrow.Meanwhile,the 12%RPS diet also increased the abundance of Firmicutes in E.coli-treated birds,along with higher production of short-chain fatty acids(SCFAs)especially propionate and butyrate.Whereas addition ofβ-acid,an inhibitor of bacterial SCFAs production,to the drinking water of ducks fed 12%RPS diet significantly decreased SCFAs level in cecum content and eliminated RPS-induced tibial mass improvement.Further,treatment with MI-2 to abrogate mucosa-associated lymphoid tissue lymphoma translocation protein 1(Malt1)activity replicated the protective role of dietary 12%RPS in E.coli-induced bone loss including reduced the inhibition on nuclear factorκB(NF-κB)inflammasome activation,decreased bone resorption,and improved bone quality,which were correlated with comparable and higher regulatory T cells(Treg)frequency in MI-2 and 12%RPS group,respectively.Conclusions:These findings suggested that the diet with 12%RPS could alleviate E.coli-induced bone loss in meat ducks by changing the gut microbial composition and promoting concomitant SCFAs production,and consequently inhibiting Malt1/NF-κB inflammasome activation and Treg cells expansion.
基金supported by the National Natural Science Foundation of China(31772622)China Agriculture Research System(CARS-42-10)+2 种基金National Key R&D Program of China(2017YFD0502004)“111”project of Foreign Experts Affairs of ChinaSichuan Agricultural University 211 Foundation.
文摘Background:Consumption of resistant starch(RS)has been associated with various intestinal and systemic health benefits,but knowledge of its effects on intestinal health and inflammatory response in stressed birds is limited.Here,we examined how dietary RS supplementation from 12%raw potato starch(RPS)modulated inflammatory severity induced by lipopolysaccharide(LPS)in meat ducks.Results:LPS administration at 14,16,and 18 d(chronic challenge)decreased body weight(BW)and glucagon-like peptide 1 receptor(GLP-1R)level with higher intestinal permeability and inflammation,evident by higher proinflammatory cytokine levels.Dietary 12%RPS supplementation enhanced Claudin-1 and GLP-1R expression,along with lower levels of inflammatory factors in both ileum and serum.Microbiome analysis showed that RS treatment shifted microbial structure reflected by enriched the proportion of Firmicutes,Bifidobacterium,Ruminococcus,etc.Dietary RS addition also significantly increased the concentrations of propionate and butyrate during chronic LPS challenge.Furthermore,response to acute challenge,the ducks received 2 mg/kg BW LPS at 14 d had higher concentrations of serum endotoxins and inflammatory cytokines,as well as upregulated transcription of toll like receptor 4(TLR4)in ileum when compared to control birds.Analogous to GLP-1 agonist liraglutide,dietary RS addition decreased endotoxins and inflammation cytokines,whereas it upregulated the GLP-1 synthesis related genes expression.Meanwhile,dietary RS supplementation suppressed the acute LPS challenge-induced TLR4 transcription.Conclusions:These data suggest that dietary 12%RPS supplementation could attenuate the LPS-induced inflammation as well as intestinal injury of meat ducks,which might involve in the alteration in gut microbiota,SCFAs production and the signaling pathways of TLR4 and GLP-1/GLP-1R.