Effects of a gluten-free diet on gut microbiota and immune function in healthy adult human subjects
Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (G...
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| Published in | British journal of nutrition Vol. 102; no. 8; pp. 1154 - 1160 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Cambridge, UK
Cambridge University Press
28.10.2009
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0007-1145 1475-2662 1475-2662 |
| DOI | 10.1017/S0007114509371767 |
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| Abstract | Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0·001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. |
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| AbstractList | Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0·001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30.3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0.007, P = 0.031 and P = 0.009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0.020, P = 0.001 and P = 0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0.005 and P = 0.003) after the GFD assessed by qPCR. TNF-alpha, interferon-gamma, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0.021, P = 0.037, P = 0.002 and P = 0.007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health.Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30.3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0.007, P = 0.031 and P = 0.009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0.020, P = 0.001 and P = 0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0.005 and P = 0.003) after the GFD assessed by qPCR. TNF-alpha, interferon-gamma, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0.021, P = 0.037, P = 0.002 and P = 0.007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions ( P = 0·001) in polysaccharides. Bifidobacterium , Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased ( P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium , Lactobacillus and Bifidobacterium longum counts decreased ( P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased ( P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced ( P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0·001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. [PUBLICATION ABSTRACT] Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30·3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0·001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0·007, P = 0·031 and P = 0·009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0·020, P = 0·001 and P = 0·017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0·005 and P = 0·003) after the GFD assessed by qPCR. TNF-α, interferon-γ, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0·021, P = 0·037, P = 0·002 and P = 0·007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30.3 years) over 1month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P=0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P=0.007, P=0.031 and P=0.009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P=0.020, P=0.001 and P=0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P=0.005 and P=0.003) after the GFD assessed by qPCR. TNF- alpha , interferon- gamma , IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P=0.021, P=0.037, P=0.002 and P=0.007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. Diet influences the composition of the gut microbiota and host's health, particularly in patients suffering from food-related diseases. Coeliac disease (CD) is a permanent intolerance to cereal gluten proteins and the only therapy for the patients is to adhere to a life-long gluten-free diet (GFD). In the present preliminary study, the effects of a GFD on the composition and immune function of the gut microbiota were analysed in ten healthy subjects (mean age 30.3 years) over 1 month. Faecal microbiota was analysed by fluorescence in situ hybridisation (FISH) and quantitative PCR (qPCR). The ability of faecal bacteria to stimulate cytokine production by peripheral blood mononuclear cells (PBMC) was determined by ELISA. No significant differences in dietary intake were found before and after the GFD except for reductions (P = 0.001) in polysaccharides. Bifidobacterium, Clostridium lituseburense and Faecalibacterium prausnitzii proportions decreased (P = 0.007, P = 0.031 and P = 0.009, respectively) as a result of the GFD analysed by FISH. Bifidobacterium, Lactobacillus and Bifidobacterium longum counts decreased (P = 0.020, P = 0.001 and P = 0.017, respectively), while Enterobacteriaceae and Escherichia coli counts increased (P = 0.005 and P = 0.003) after the GFD assessed by qPCR. TNF-alpha, interferon-gamma, IL-10 and IL-8 production by PBMC stimulated with faecal samples was also reduced (P = 0.021, P = 0.037, P = 0.002 and P = 0.007, respectively) after the diet. Therefore, the GFD led to reductions in beneficial gut bacteria populations and the ability of faecal samples to stimulate the host's immunity. Thus, the GFD may constitute an environmental variable to be considered in treated CD patients for its possible effects on gut health. |
| Author | Collado, Maria Carmen De Palma, Giada Nadal, Inmaculada Sanz, Yolanda |
| Author_xml | – sequence: 1 givenname: Giada surname: De Palma fullname: De Palma, Giada organization: Microbial Ecophysiology and Nutrition Group, Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain – sequence: 2 givenname: Inmaculada surname: Nadal fullname: Nadal, Inmaculada organization: Microbial Ecophysiology and Nutrition Group, Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain – sequence: 3 givenname: Maria Carmen surname: Collado fullname: Collado, Maria Carmen organization: Microbial Ecophysiology and Nutrition Group, Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain – sequence: 4 givenname: Yolanda surname: Sanz fullname: Sanz, Yolanda email: yolsanz@iata.csic.es organization: Microbial Ecophysiology and Nutrition Group, Institute of Agrochemistry and Food Technology (IATA), Spanish National Research Council (CSIC), PO Box 73, 46100 Burjassot, Valencia, Spain |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22036572$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/19445821$$D View this record in MEDLINE/PubMed |
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| Keywords | Gluten-free diet Coeliac disease Immunity Intestinal microbiota Human Immunopathology Healthy subject Digestive system Gut Microflora Feeding Vertebrata Mammalia Diet Intestinal malabsorption Digestive diseases Intestinal disease Adult Gluten |
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| References | Sanz (S0007114509371767_ref8) 2008 Farran (S0007114509371767_ref10) 2004 Langendijk (S0007114509371767_ref14) 1995; 61 S0007114509371767_ref2 S0007114509371767_ref1 S0007114509371767_ref4 S0007114509371767_ref19 S0007114509371767_ref3 S0007114509371767_ref16 S0007114509371767_ref6 S0007114509371767_ref5 S0007114509371767_ref7 Franks (S0007114509371767_ref18) 1998; 64 S0007114509371767_ref9 S0007114509371767_ref30 Amann (S0007114509371767_ref12) 1990; 56 S0007114509371767_ref31 S0007114509371767_ref15 S0007114509371767_ref13 Collado (S0007114509371767_ref11) 2007; 8 Poulsen (S0007114509371767_ref17) 1994; 62 S0007114509371767_ref29 S0007114509371767_ref27 S0007114509371767_ref28 S0007114509371767_ref21 S0007114509371767_ref22 S0007114509371767_ref20 S0007114509371767_ref25 S0007114509371767_ref26 S0007114509371767_ref23 S0007114509371767_ref24 20465858 - Br J Nutr. 2010 Sep;104(5):773 |
| References_xml | – ident: S0007114509371767_ref21 doi: 10.1002/cyto.990140205 – volume: 64 start-page: 3336 year: 1998 ident: S0007114509371767_ref18 article-title: Variations of bacterial populations in human faeces measured by fluorescent in situ hybridization with group specific 16S rRNA-targeted oligonucleotide probes publication-title: Appl Environ Microbiol doi: 10.1128/AEM.64.9.3336-3345.1998 – ident: S0007114509371767_ref9 doi: 10.1007/s10803-006-0079-0 – ident: S0007114509371767_ref31 doi: 10.1016/S0065-2776(08)60449-6 – ident: S0007114509371767_ref26 doi: 10.1038/sj.ejcn.1602856 – ident: S0007114509371767_ref24 doi: 10.1099/mic.0.25975-0 – ident: S0007114509371767_ref2 doi: 10.1038/nri885 – ident: S0007114509371767_ref27 doi: 10.1016/S0065-2911(07)53002-X – ident: S0007114509371767_ref5 doi: 10.1016/j.cgh.2007.12.022 – ident: S0007114509371767_ref22 doi: 10.1016/j.vetmic.2006.12.006 – volume: 62 start-page: 5191 year: 1994 ident: S0007114509371767_ref17 article-title: Spatial distribution of Escherichia coli in the mouse large intestine inferred from rRNA in situ hybridization publication-title: Infect Immun doi: 10.1128/IAI.62.11.5191-5194.1994 – volume: 61 start-page: 3069 year: 1995 ident: S0007114509371767_ref14 article-title: Quantitative fluorescence in situ hybridization of Bifidobacterium spp. with genus specific 16S rRNA-targeted probes and its application in fecal samples publication-title: Appl Environ Microbiol doi: 10.1128/AEM.61.8.3069-3075.1995 – volume: 56 start-page: 1919 year: 1990 ident: S0007114509371767_ref12 article-title: Combination of 16S rRNA-targeted oligonucleotide probes with flow cytometry for analyzing mixed microbial populations publication-title: Appl Environ Microbiol doi: 10.1128/AEM.56.6.1919-1925.1990 – ident: S0007114509371767_ref3 doi: 10.1016/j.imlet.2005.02.017 – ident: S0007114509371767_ref25 doi: 10.1111/j.1365-2249.2007.03522.x – ident: S0007114509371767_ref4 doi: 10.1007/s10875-006-9061-z – ident: S0007114509371767_ref1 doi: 10.1016/0016-5085(92)91819-P – volume-title: Tablas de Composición de Alimentos CESNID (CESNID Food Composition Tables) year: 2004 ident: S0007114509371767_ref10 – ident: S0007114509371767_ref19 doi: 10.1128/AEM.69.7.4320-4324.2003 – ident: S0007114509371767_ref20 doi: 10.1078/0723-2020-00015 – ident: S0007114509371767_ref15 doi: 10.1111/j.1574-6968.2000.tb08945.x – ident: S0007114509371767_ref16 doi: 10.1099/13500872-142-5-1097 – ident: S0007114509371767_ref23 doi: 10.1128/AEM.68.11.5445-5451.2002 – ident: S0007114509371767_ref7 doi: 10.1099/jmm.0.47410-0 – ident: S0007114509371767_ref6 doi: 10.1159/000116770 – ident: S0007114509371767_ref30 doi: 10.1073/pnas.212527599 – ident: S0007114509371767_ref29 doi: 10.1002/ibd.20330 – volume: 8 start-page: 9 year: 2007 ident: S0007114509371767_ref11 article-title: Differences between the fecal microbiota of coeliac infants and healthy controls publication-title: Curr Issues Intest Microbiol – ident: S0007114509371767_ref28 doi: 10.1136/jcp.2008.061366 – ident: S0007114509371767_ref13 doi: 10.1128/AEM.66.10.4523-4527.2000 – start-page: 210 volume-title: Child Nutrition and Physiology year: 2008 ident: S0007114509371767_ref8 – reference: 20465858 - Br J Nutr. 2010 Sep;104(5):773 |
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