The Experts below are selected from a list of 1704 Experts worldwide ranked by ideXlab platform
Eugene B Chang - One of the best experts on this subject based on the ideXlab platform.
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pathobiont and colitis in IL-10−/ − mice
2016Co-Authors: Suzanne Devkota, Yunwei Wang, Vanessa Leone, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Mark Musch, Hannah Fehlner-peach, Eugene B ChangAbstract:fat-induced Taurocholic Acid production promote
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health 1 . Here we show that consumption of a diet high in saturated (milkderived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia 2 . This was associated with a pro-inflammatory T helper type 1( T H1) immune response and increased incidence of colitis in genetically susceptible Il10 2/2 , but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10 2/2 mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immunemediated diseases like inflammatory bowel disease in genetically susceptible hosts. Inflammatory bowel diseases (IBD) and other immune-related human disorders are relatively ‘new’ diseases in that their incidence has increased considerably over the past half century, matching developments in cultural westernization 1,3,4 . The rapidity of these developments are probably not caused by genetic drift, but by exposure to non-genetic factors introduced through changes in the diet and lifestyle of genetically susceptible individuals, triggering aberrant host responses that lead to IBD. In this study, we examine whether certain dietary fats present in Western diets are capable of precipitating colonic inflammation through their actions on the enteric microbiota of genetically susceptible hosts. The effects of three different diets (Supplementary Table 1) on the enteric microbiota of specific-pathogen-free (SPF) C57BL/6 mice are shown in Fig. 1a and Supplementary Table 2. With the exception of the low-fat purified mouse diet (LF), the high-fat diets were isocaloric and differed only in the type of dietary fat used, which was held constant at 37% of total calories and closely mimics Western consumption 5 . These fats also represent sources used in numerous processed
Suzanne Devkota - One of the best experts on this subject based on the ideXlab platform.
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pathobiont and colitis in IL-10−/ − mice
2016Co-Authors: Suzanne Devkota, Yunwei Wang, Vanessa Leone, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Mark Musch, Hannah Fehlner-peach, Eugene B ChangAbstract:fat-induced Taurocholic Acid production promote
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health 1 . Here we show that consumption of a diet high in saturated (milkderived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia 2 . This was associated with a pro-inflammatory T helper type 1( T H1) immune response and increased incidence of colitis in genetically susceptible Il10 2/2 , but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10 2/2 mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immunemediated diseases like inflammatory bowel disease in genetically susceptible hosts. Inflammatory bowel diseases (IBD) and other immune-related human disorders are relatively ‘new’ diseases in that their incidence has increased considerably over the past half century, matching developments in cultural westernization 1,3,4 . The rapidity of these developments are probably not caused by genetic drift, but by exposure to non-genetic factors introduced through changes in the diet and lifestyle of genetically susceptible individuals, triggering aberrant host responses that lead to IBD. In this study, we examine whether certain dietary fats present in Western diets are capable of precipitating colonic inflammation through their actions on the enteric microbiota of genetically susceptible hosts. The effects of three different diets (Supplementary Table 1) on the enteric microbiota of specific-pathogen-free (SPF) C57BL/6 mice are shown in Fig. 1a and Supplementary Table 2. With the exception of the low-fat purified mouse diet (LF), the high-fat diets were isocaloric and differed only in the type of dietary fat used, which was held constant at 37% of total calories and closely mimics Western consumption 5 . These fats also represent sources used in numerous processed
Yunwei Wang - One of the best experts on this subject based on the ideXlab platform.
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pathobiont and colitis in IL-10−/ − mice
2016Co-Authors: Suzanne Devkota, Yunwei Wang, Vanessa Leone, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Mark Musch, Hannah Fehlner-peach, Eugene B ChangAbstract:fat-induced Taurocholic Acid production promote
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health 1 . Here we show that consumption of a diet high in saturated (milkderived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia 2 . This was associated with a pro-inflammatory T helper type 1( T H1) immune response and increased incidence of colitis in genetically susceptible Il10 2/2 , but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10 2/2 mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immunemediated diseases like inflammatory bowel disease in genetically susceptible hosts. Inflammatory bowel diseases (IBD) and other immune-related human disorders are relatively ‘new’ diseases in that their incidence has increased considerably over the past half century, matching developments in cultural westernization 1,3,4 . The rapidity of these developments are probably not caused by genetic drift, but by exposure to non-genetic factors introduced through changes in the diet and lifestyle of genetically susceptible individuals, triggering aberrant host responses that lead to IBD. In this study, we examine whether certain dietary fats present in Western diets are capable of precipitating colonic inflammation through their actions on the enteric microbiota of genetically susceptible hosts. The effects of three different diets (Supplementary Table 1) on the enteric microbiota of specific-pathogen-free (SPF) C57BL/6 mice are shown in Fig. 1a and Supplementary Table 2. With the exception of the low-fat purified mouse diet (LF), the high-fat diets were isocaloric and differed only in the type of dietary fat used, which was held constant at 37% of total calories and closely mimics Western consumption 5 . These fats also represent sources used in numerous processed
Vanessa Leone - One of the best experts on this subject based on the ideXlab platform.
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pathobiont and colitis in IL-10−/ − mice
2016Co-Authors: Suzanne Devkota, Yunwei Wang, Vanessa Leone, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Mark Musch, Hannah Fehlner-peach, Eugene B ChangAbstract:fat-induced Taurocholic Acid production promote
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health 1 . Here we show that consumption of a diet high in saturated (milkderived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia 2 . This was associated with a pro-inflammatory T helper type 1( T H1) immune response and increased incidence of colitis in genetically susceptible Il10 2/2 , but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10 2/2 mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immunemediated diseases like inflammatory bowel disease in genetically susceptible hosts. Inflammatory bowel diseases (IBD) and other immune-related human disorders are relatively ‘new’ diseases in that their incidence has increased considerably over the past half century, matching developments in cultural westernization 1,3,4 . The rapidity of these developments are probably not caused by genetic drift, but by exposure to non-genetic factors introduced through changes in the diet and lifestyle of genetically susceptible individuals, triggering aberrant host responses that lead to IBD. In this study, we examine whether certain dietary fats present in Western diets are capable of precipitating colonic inflammation through their actions on the enteric microbiota of genetically susceptible hosts. The effects of three different diets (Supplementary Table 1) on the enteric microbiota of specific-pathogen-free (SPF) C57BL/6 mice are shown in Fig. 1a and Supplementary Table 2. With the exception of the low-fat purified mouse diet (LF), the high-fat diets were isocaloric and differed only in the type of dietary fat used, which was held constant at 37% of total calories and closely mimics Western consumption 5 . These fats also represent sources used in numerous processed
Anuradha Nadimpalli - One of the best experts on this subject based on the ideXlab platform.
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pathobiont and colitis in IL-10−/ − mice
2016Co-Authors: Suzanne Devkota, Yunwei Wang, Vanessa Leone, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Mark Musch, Hannah Fehlner-peach, Eugene B ChangAbstract:fat-induced Taurocholic Acid production promote
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia. This was associated with a pro-inflammatory T helper type 1 (T(H)1) immune response and increased incidence of colitis in genetically susceptible Il10(−/−), but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10(−/−) mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.
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dietary fat induced Taurocholic Acid promotes pathobiont expansion and colitis in il10 mice
Nature, 2012Co-Authors: Suzanne Devkota, Yunwei Wang, Mark W Musch, Vanessa Leone, Hannah Fehlnerpeach, Anuradha Nadimpalli, Dionysios A Antonopoulos, Bana Jabri, Eugene B ChangAbstract:The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health 1 . Here we show that consumption of a diet high in saturated (milkderived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia 2 . This was associated with a pro-inflammatory T helper type 1( T H1) immune response and increased incidence of colitis in genetically susceptible Il10 2/2 , but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile Acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with Taurocholic Acid, but not with glycocholic Acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10 2/2 mice. Together these data show that dietary fats, by promoting changes in host bile Acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immunemediated diseases like inflammatory bowel disease in genetically susceptible hosts. Inflammatory bowel diseases (IBD) and other immune-related human disorders are relatively ‘new’ diseases in that their incidence has increased considerably over the past half century, matching developments in cultural westernization 1,3,4 . The rapidity of these developments are probably not caused by genetic drift, but by exposure to non-genetic factors introduced through changes in the diet and lifestyle of genetically susceptible individuals, triggering aberrant host responses that lead to IBD. In this study, we examine whether certain dietary fats present in Western diets are capable of precipitating colonic inflammation through their actions on the enteric microbiota of genetically susceptible hosts. The effects of three different diets (Supplementary Table 1) on the enteric microbiota of specific-pathogen-free (SPF) C57BL/6 mice are shown in Fig. 1a and Supplementary Table 2. With the exception of the low-fat purified mouse diet (LF), the high-fat diets were isocaloric and differed only in the type of dietary fat used, which was held constant at 37% of total calories and closely mimics Western consumption 5 . These fats also represent sources used in numerous processed
