DOP076. Impact of western diet on short-chain fatty acids production and host susceptibility to intestinal inflammation in a context of Crohn's Disease

Abstract Background Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD. Methods Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota. Results Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. Certain relationships differed between patients and controls and by sex. Conclusions Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson's disease

10.21203/rs.3.rs-63018/v1 ◽

2020 ◽

Author(s):

Velma T Aho ◽

Madelyn Crawford Houser ◽

Pedro AB Pereira ◽

Jianjun Chang ◽

Knut Rudi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Fatty Acids ◽

Parkinson's Disease ◽

Gut Microbiota ◽

Intestinal Inflammation ◽

Disease Onset ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

Abstract Background: Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD.Methods: Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota.Results: Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. Certain relationships differed between patients and controls and by sex.Conclusions: Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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Salmonella versus the Microbiome

Microbiology and Molecular Biology Reviews ◽

10.1128/mmbr.00027-19 ◽

2020 ◽

Vol 85 (1) ◽

pp. e00027-19

Author(s):

Andrew W. L. Rogers ◽

Renée M. Tsolis ◽

Andreas J. Bäumler

Keyword(s):

Fatty Acids ◽

Intestinal Inflammation ◽

Opportunistic Infections ◽

Short Chain Fatty Acids ◽

Fecal Microbiota ◽

Short Chain ◽

Noncommunicable Diseases ◽

Colonization Resistance ◽

Habitat Filtering ◽

Chain Fatty Acids

SUMMARYA balanced gut microbiota contributes to health, but the mechanisms maintaining homeostasis remain elusive. Microbiota assembly during infancy is governed by competition between species and by environmental factors, termed habitat filters, that determine the range of successful traits within the microbial community. These habitat filters include the diet, host-derived resources, and microbiota-derived metabolites, such as short-chain fatty acids. Once the microbiota has matured, competition and habitat filtering prevent engraftment of new microbes, thereby providing protection against opportunistic infections. Competition with endogenous Enterobacterales, habitat filtering by short-chain fatty acids, and a host-derived habitat filter, epithelial hypoxia, also contribute to colonization resistance against Salmonella serovars. However, at a high challenge dose, these frank pathogens can overcome colonization resistance by using their virulence factors to trigger intestinal inflammation. In turn, inflammation increases the luminal availability of host-derived resources, such as oxygen, nitrate, tetrathionate, and lactate, thereby creating a state of abnormal habitat filtering that enables the pathogen to overcome growth inhibition by short-chain fatty acids. Thus, studying the process of ecosystem invasion by Salmonella serovars clarifies that colonization resistance can become weakened by disrupting host-mediated habitat filtering. This insight is relevant for understanding how inflammation triggers dysbiosis linked to noncommunicable diseases, conditions in which endogenous Enterobacterales expand in the fecal microbiota using some of the same growth-limiting resources required by Salmonella serovars for ecosystem invasion. In essence, ecosystem invasion by Salmonella serovars suggests that homeostasis and dysbiosis simply represent states where competition and habitat filtering are normal or abnormal, respectively.

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Short-chain fatty acids and intestinal inflammation in Multiple Sclerosis – Modulation of female susceptibility by microbial products?

10.21203/rs.3.rs-85998/v1 ◽

2020 ◽

Author(s):

Anouck Becker ◽

Mosab Abuazab ◽

Andreas Schwiertz ◽

Silke Walter ◽

Klaus C. Faßbender ◽

...

Keyword(s):

Multiple Sclerosis ◽

Fatty Acids ◽

Intestinal Inflammation ◽

Short Chain Fatty Acids ◽

Fecal Calprotectin ◽

Short Chain ◽

Therapeutic Regime ◽

Microbial Products ◽

Chain Fatty Acids

Abstract Background. Multiple Sclerosis (MS) is an autoimmune-mediated disease of the central nervous system. Experimental data also suggest a role of intestinal microbiota and microbial products such as short-chain fatty acids (SCFA) in the pathogenesis of MS. A recent clinical study reported beneficial effects (mediated by immunomodulatory mechanisms) after oral administration of the SCFA propionate in MS patients. Based on available evidence, we aimed to investigate whether SCFA and the fecal inflammation marker calprotectin are altered in MS. Methods. 76 subjects (41 patients with relapsing-remitting MS and 35 age-matched controls) were investigated in this case-control study. All subjects underwent clinical assessment with established scales and provided fecal samples for a quantitative analysis of fecal SCFA and fecal calprotectin concentration. Fecal markers were compared between MS patients and controls, and were analyzed for an association with epidemiological as well as clinical parameters. Results. Median fecal calprotectin concentrations remained within normal range without any group-specific differences. Fecal SCFA showed a non-significant reduction in MS patients, whereas female subjects showed significantly reduced SCFA concentrations compared to male subjects. Conclusions. In our cohort of MS patients, we found no evidence of an active intestinal inflammation. As the vast majority of patients, however, was under immunotherapy, this might have affected the outcome measures. The sex-associated difference in fecal SCFA concentrations might at least partially explain female predominance in MS. Large-scale longitudinal studies including drug-naïve MS patients are required to determine the role of SCFA in MS and to distinguish between disease-immanent effects and those caused by the therapeutic regime.

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Relationships of gut microbiota, short-chain fatty acids, inflammation, and the gut barrier in Parkinson’s disease

10.1101/2020.06.15.20131011 ◽

2020 ◽

Author(s):

Velma T. E. Aho ◽

Madelyn C. Houser ◽

Pedro A. B. Pereira ◽

Jianjun Chang ◽

Knut Rudi ◽

...

Keyword(s):

Parkinson’S Disease ◽

Fatty Acids ◽

Parkinson's Disease ◽

Gut Microbiota ◽

Intestinal Inflammation ◽

Disease Onset ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Dependent Manner ◽

Chain Fatty Acids

AbstractBackgroundPrevious studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and contribute to disease processes and symptoms remains uncertain.ObjectivesThis study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD.MethodsStool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota.ResultsCalprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of stool SCFAs, inflammation, and zonulin. These relationships differed somewhat between patients and controls and by sex.ConclusionsIntestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are PD- and sex-dependent. Alterations in microbiota-host interactions and links between intestinal inflammation and reduced SCFA levels and earlier PD onset warrant further investigation.

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Fatty Acid Profile of Synbiotic Cheese and its Effect on Intestinal Inflammation in Rats

International Journal of Probiotics and Prebiotics ◽

10.37290/ijpp2641-7197.14:45-50 ◽

2019 ◽

Vol 14 (1) ◽

pp. 45-50

Author(s):

Nurliyani ◽

Harmayani Eni ◽

Rahmatulloh Satyaguna ◽

Rakasivi Kanita Galih Julia

Keyword(s):

Fatty Acids ◽

Lactic Acid ◽

Fatty Acid ◽

Lactic Acid Bacteria ◽

Fatty Acid Profile ◽

Intestinal Inflammation ◽

Lactobacillus Rhamnosus ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Chain Fatty Acids

Porang (Amorphophallus oncophyllus) is a local perennial plant rich in glucomannan. The objective of this study was to determine the effect of porang glucomannan addition during cheese processing on fatty acid profile, organic acid and vitamin B6 of goat milk cheese ripened with Lactobacillus rhamnosus. In addition, the effect of cheese consumption on short-chain fatty acid profile in the caecum digesta of inflammatory rats was evaluated. We found that the addition of glucomannan to the cheese during its ripening increased the levels of myristic, pentadecanoic acid, and cis-oleic acids. Rats consuming this cheese had elevated cecal levels of propionic, butyric, total short-chain fatty acids, and lactic acid bacteria. Consumption of synbiotic cheese also decreased the intestinal inflammation via increasing the total lactic acid bacteria, propionic, butyric, and total short-chain fatty acids.

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In search for interplay between stool microRNAs, microbiota and short chain fatty acids in Crohn’s disease - a preliminary study

BMC Gastroenterology ◽

10.1186/s12876-020-01444-3 ◽

2020 ◽

Vol 20 (1) ◽

Cited By ~ 1

Author(s):

Filip Ambrozkiewicz ◽

Jakub Karczmarski ◽

Maria Kulecka ◽

Agnieszka Paziewska ◽

Magdalena Niemira ◽

...

Keyword(s):

Crohn’S Disease ◽

Crohn's Disease ◽

Large Scale ◽

Intestinal Inflammation ◽

Short Chain Fatty Acids ◽

Short Chain ◽

Inactive Disease ◽

Targeted Analysis ◽

Α Diversity ◽

Bowel Diseases

Abstract Background Inflammatory bowel diseases are classic polygenic disorders, with genetic loads that reflect immunopathological processes in response to the intestinal microbiota. Herein we performed the multiomics analysis by combining the large scale surveys of gut bacterial community, stool microRNA (miRNA) and short chain fatty acid (SCFA) signatures to correlate their association with the activity of Crohn’s disease (CD). Methods DNA, miRNA, and metabolites were extracted from stool samples of 15 CD patients, eight with active disease and seven in remission, and nine healthy individuals. Microbial, miRNA and SCFA profiles were assessed using datasets from 16S rRNA sequencing, Nanostring miRNA and GC-MS targeted analysis, respectively. Results Pairwise comparisons showed that 9 and 23 taxa differed between controls and CD patients with active and inactive disease, respectively. Six taxa were common to both comparisons, whereas four taxa differed in CD patients. α-Diversity was lower in both CD groups than in controls. The levels of 13 miRNAs differed (p-value < 0.05; FC > 1.5) in CD patients and controls before FDR correction and 4 after. Of six SCFAs, the levels of two differed significantly (p-value < 0.05, FC > 1.5) in CD patients and controls, and the levels of four differed in patients with active and inactive CD. PLS-DA revealed models with smallest error rate for controls in bacterial component and inactive disease in metabolites. Conclusion A complex interrelationship may exist between gut dysbiosis, miRNA profiling and SCFA level in response to intestinal inflammation.

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