Background Coccidiosis,caused by Eimeria parasites,is a major enteric disease in poultry,significantly impacting animal health,production performance,and welfare.This disease imposes a substantial economic burden,cost...Background Coccidiosis,caused by Eimeria parasites,is a major enteric disease in poultry,significantly impacting animal health,production performance,and welfare.This disease imposes a substantial economic burden,costing the global poultry industry up to$13 billion annually.However,effective mitigation strategies for coccidiosis remain elusive.While different chicken breeds exhibit varying resistance to coccidiosis,no commensal bacteria have been directly linked to this resistance.Methods To assess relative resistance of different breeds to coccidiosis,10-day-old Fayoumi M5.1,Leghorn Ghs6,and Cobb chickens were challenged with 50,000 sporulated Eimeria maxima oocysts or mock-infected.Body weight changes,small intestinal lesions,and fecal oocyst shedding were evaluated on d 17.Ileal and cecal digesta were collected from individual animals on d 17 and subjected to microbiome analysis using 16S rRNA gene sequencing.Results Fayoumi M5.1 chickens showed the lowest growth retardation,intestinal lesion score,fecal oocyst shedding,and pathobiont proliferation compared to Ghs6 and Cobb chickens.The intestinal microbiota of M5.1 chickens also differed markedly from the other two breeds under both healthy and coccidiosis conditions.Notably,group A Lactobacillus and Ligilactobacillus salivarius were the least prevalent in both the ileum and cecum of healthy M5.1 chickens,but became highly enriched and comparable to Ghs6 and Cobb chickens in response to coccidiosis.Conversely,Weissella,Staphylococcus gallinarum,and Enterococcus durans/hirae were more abundant in the ileum of healthy M5.1 chickens than in the other two breeds.Despite being reduced by Eimeria,these bacteria retained higher abundance in M5.1 chickens compared to the other breeds.Conclusions Fayoumi M5.1 chickens exhibit greater resistance to coccidiosis than Leghorn Ghs6 layers and Cobb broilers.Several commensal bacteria,including group A Lactobacillus,L.salivarius,Weissella,S.gallinarum,and E.durans/hirae,are differentially enriched in Fayoumi M5.1 chickens with strong correlation with coccidiosis resistance.These bacteria hold potential as probiotics for coccidiosis mitigation.展开更多
Background Necrotic enteritis(NE)is a major enteric disease in poultry,yet effective mitigation strategies remain elusive.Deoxycholic acid(DCA)and butyrate,two major metabolites derived from the intestinal microbiota,...Background Necrotic enteritis(NE)is a major enteric disease in poultry,yet effective mitigation strategies remain elusive.Deoxycholic acid(DCA)and butyrate,two major metabolites derived from the intestinal microbiota,have independently been shown to induce host defense peptide(HDP)synthesis.However,the potential synergy between these two compounds remains unexplored.Methods To investigate the possible synergistic effect between DCA and butyrate in regulating HDP synthesis and barrier function,we treated chicken HD11 macrophage cells and jejunal explants with DCA and sodium butyrate(NaB),either individually or in combination,for 24 h.Subsequently,we performed RNA isolation and reverse transcrip-tion-quantitative PCR to analyze HDP genes as well as the major genes associated with barrier function.To further determine the synergy between DCA and NaB in enhancing NE resistance,we conducted two independent trials with Cobb broiler chicks.In each trial,the diet was supplemented with DCA or NaB on the day-of-hatch,followed by NE induction through sequential challenges with Eimeria maxima and Clostridium perfringens on d 10 and 14,respectively.We recorded animal mortality after infection and assessed intestinal lesions on d 17.The impact of DCA and NaB on the microbiota in the ileum and cecum was evaluated through bacterial 16S rRNA gene sequencing.Results We found that the combination of DCA and NaB synergistically induced multiple HDP genes in both chicken HD11 cells and jejunal explants.Additionally,the gene for claudin-1,a major tight junction protein,also exhibited synergistic induction in response to DCA and NaB.Furthermore,dietary supplementation with a combination of 0.75 g/kg DCA and 1 g/kg NaB led to a significant improvement in animal survival and a reduction in intestinal lesions compared to either compound alone in a chicken model of NE.Notably,the cecal microbiota of NE-infected chickens showed a marked decrease in SCFA-producing bacteria such as Bacteroides,Faecalibacterium,and Cuneatibacter,with lactobacilli becoming the most dominant species.However,supplementation with DCA and NaB largely restored the intestinal microbiota to healthy levels.Conclusions DCA synergizes with NaB to induce HDP and claudin-1 expression and enhance NE resistance,with potential for further development as cost-effective antibiotic alternatives.展开更多
基金funded by the USDA National Institute of Food and Agriculture grants(2022-67016-37208 and 2024-67016-42415)the Ralph F.and Leila W.Boulware Endowment Fund,Oklahoma Agricultural Experiment Station Project H-3268+1 种基金Iowa Agriculture and Home Economics Experiment Station Project IOW05620supported by two separate USDA National Institute of Food and Agriculture Predoctoral Fellowship grants(2024-67011-42944 and 2021-67034-35184).
文摘Background Coccidiosis,caused by Eimeria parasites,is a major enteric disease in poultry,significantly impacting animal health,production performance,and welfare.This disease imposes a substantial economic burden,costing the global poultry industry up to$13 billion annually.However,effective mitigation strategies for coccidiosis remain elusive.While different chicken breeds exhibit varying resistance to coccidiosis,no commensal bacteria have been directly linked to this resistance.Methods To assess relative resistance of different breeds to coccidiosis,10-day-old Fayoumi M5.1,Leghorn Ghs6,and Cobb chickens were challenged with 50,000 sporulated Eimeria maxima oocysts or mock-infected.Body weight changes,small intestinal lesions,and fecal oocyst shedding were evaluated on d 17.Ileal and cecal digesta were collected from individual animals on d 17 and subjected to microbiome analysis using 16S rRNA gene sequencing.Results Fayoumi M5.1 chickens showed the lowest growth retardation,intestinal lesion score,fecal oocyst shedding,and pathobiont proliferation compared to Ghs6 and Cobb chickens.The intestinal microbiota of M5.1 chickens also differed markedly from the other two breeds under both healthy and coccidiosis conditions.Notably,group A Lactobacillus and Ligilactobacillus salivarius were the least prevalent in both the ileum and cecum of healthy M5.1 chickens,but became highly enriched and comparable to Ghs6 and Cobb chickens in response to coccidiosis.Conversely,Weissella,Staphylococcus gallinarum,and Enterococcus durans/hirae were more abundant in the ileum of healthy M5.1 chickens than in the other two breeds.Despite being reduced by Eimeria,these bacteria retained higher abundance in M5.1 chickens compared to the other breeds.Conclusions Fayoumi M5.1 chickens exhibit greater resistance to coccidiosis than Leghorn Ghs6 layers and Cobb broilers.Several commensal bacteria,including group A Lactobacillus,L.salivarius,Weissella,S.gallinarum,and E.durans/hirae,are differentially enriched in Fayoumi M5.1 chickens with strong correlation with coccidiosis resistance.These bacteria hold potential as probiotics for coccidiosis mitigation.
基金supported by the USDA National Institute of Food and Agriculture grants (2020-67016-31619 and 2023-67015-39095)the Ralph F. and Leila W. Boulware Endowment Fund+1 种基金Oklahoma Agricultural Experiment Station Project H-3112supported by a USDA National Institute of Food and Agriculture Predoctoral Fellowship grant (2021-67034-35184)
文摘Background Necrotic enteritis(NE)is a major enteric disease in poultry,yet effective mitigation strategies remain elusive.Deoxycholic acid(DCA)and butyrate,two major metabolites derived from the intestinal microbiota,have independently been shown to induce host defense peptide(HDP)synthesis.However,the potential synergy between these two compounds remains unexplored.Methods To investigate the possible synergistic effect between DCA and butyrate in regulating HDP synthesis and barrier function,we treated chicken HD11 macrophage cells and jejunal explants with DCA and sodium butyrate(NaB),either individually or in combination,for 24 h.Subsequently,we performed RNA isolation and reverse transcrip-tion-quantitative PCR to analyze HDP genes as well as the major genes associated with barrier function.To further determine the synergy between DCA and NaB in enhancing NE resistance,we conducted two independent trials with Cobb broiler chicks.In each trial,the diet was supplemented with DCA or NaB on the day-of-hatch,followed by NE induction through sequential challenges with Eimeria maxima and Clostridium perfringens on d 10 and 14,respectively.We recorded animal mortality after infection and assessed intestinal lesions on d 17.The impact of DCA and NaB on the microbiota in the ileum and cecum was evaluated through bacterial 16S rRNA gene sequencing.Results We found that the combination of DCA and NaB synergistically induced multiple HDP genes in both chicken HD11 cells and jejunal explants.Additionally,the gene for claudin-1,a major tight junction protein,also exhibited synergistic induction in response to DCA and NaB.Furthermore,dietary supplementation with a combination of 0.75 g/kg DCA and 1 g/kg NaB led to a significant improvement in animal survival and a reduction in intestinal lesions compared to either compound alone in a chicken model of NE.Notably,the cecal microbiota of NE-infected chickens showed a marked decrease in SCFA-producing bacteria such as Bacteroides,Faecalibacterium,and Cuneatibacter,with lactobacilli becoming the most dominant species.However,supplementation with DCA and NaB largely restored the intestinal microbiota to healthy levels.Conclusions DCA synergizes with NaB to induce HDP and claudin-1 expression and enhance NE resistance,with potential for further development as cost-effective antibiotic alternatives.
