Fecal microbiota in congenital chloride diarrhea and inflammatory bowel disease

Background and aimsSubjects with congenital chloride diarrhea (CLD; a defect in solute carrier family 26 member 3 (SLC26A3)) are prone to inflammatory bowel disease (IBD). We investigated fecal microbiota in CLD and CLD-associated IBD. We also tested whether microbiota is modulated by supplementation with the short-chain fatty acid butyrate.Subjects and methodsWe recruited 30 patients with CLD for an observational 3-week follow-up study. Thereafter, 16 consented to oral butyrate substitution for a 3-week observational period. Fecal samples, collected once a week, were assayed for calprotectin and potential markers of inflammation, and studied by 16S ribosomal ribonucleic acid (rRNA) gene amplicon sequencing and compared to that of 19 healthy controls and 43 controls with Crohn's disease. Data on intestinal symptoms, diet and quality of life were collected.ResultsPatients with CLD had increased abundances of Proteobacteria, Veillonella, and Prevotella, and lower abundances of normally dominant taxa Ruminococcaceae and Lachnospiraceae when compared with healthy controls and Crohn's disease. No major differences in fecal microbiota were found between CLD and CLD-associated IBD (including two with yet untreated IBD). Butyrate was poorly tolerated and showed no major effects on fecal microbiota or biomarkers in CLD.ConclusionsFecal microbiota in CLD is different from that of healthy subjects or Crohn's disease. Unexpectedly, no changes in the microbiota or fecal markers characterized CLD-associated IBD, an entity with high frequency among patients with CLD.Peer reviewe

Dzemdību laikā mātes saņemtās antibakteriālās terapijas ietekme uz jaundzimušā un mātes zarnu trakta mikrobiotu

MedicīnaVeselības aprūpeMedicineHealth CareBackground and aims Subjects with congenital chloride diarrhea (CLD; a defect in solute carrier family 26 member 3 (SLC26A3)) are prone to inflammatory bowel disease (IBD). I investigated fecal microbiota in CLD. I also tested whether microbiota is modulated by supplementation with the short-chain fatty acid butyrate. Subjects and methods I recruited 8 patients under 18-years-old with CLD for an observational 3-week follow- up study. Thereafter, two of the children consented to oral butyrate substitution for a 3-week observational period. Fecal samples, collected once a week, were assayed for calprotectin and potential markers of inflammation, and studied by 16S ribosomal ribonucleic acid (rRNA) gene amplicon sequencing and compared to that of 19 healthy controls. Data on intestinal symptoms, diet and quality of life were collected. Conclusions Fecal microbiota is different between groups of CLD children (< 10-years of age), CLD adolescents (12-16-years of age) and healthy adult controls. Butyrate was poorly tolerated and showed no major effects on fecal microbiota or biomarkers in CLD.Background and aims Subjects with congenital chloride diarrhea (CLD; a defect in solute carrier family 26 member 3 (SLC26A3)) are prone to inflammatory bowel disease (IBD). I investigated fecal microbiota in CLD. I also tested whether microbiota is modulated by supplementation with the short-chain fatty acid butyrate. Subjects and methods I recruited 8 patients under 18-years-old with CLD for an observational 3-week follow- up study. Thereafter, two of the children consented to oral butyrate substitution for a 3-week observational period. Fecal samples, collected once a week, were assayed for calprotectin and potential markers of inflammation, and studied by 16S ribosomal ribonucleic acid (rRNA) gene amplicon sequencing and compared to that of 19 healthy controls. Data on intestinal symptoms, diet and quality of life were collected. Conclusions Fecal microbiota is different between groups of CLD children (< 10-years of age), CLD adolescents (12-16-years of age) and healthy adult controls. Butyrate was poorly tolerated and showed no major effects on fecal microbiota or biomarkers in CLD

Fecal microbiota in congenital chloride diarrhea and inflammatory bowel disease

Background and aimsSubjects with congenital chloride diarrhea (CLD; a defect in solute carrier family 26 member 3 (SLC26A3)) are prone to inflammatory bowel disease (IBD). We investigated fecal microbiota in CLD and CLD-associated IBD. We also tested whether microbiota is modulated by supplementation with the short-chain fatty acid butyrate.Subjects and methodsWe recruited 30 patients with CLD for an observational 3-week follow-up study. Thereafter, 16 consented to oral butyrate substitution for a 3-week observational period. Fecal samples, collected once a week, were assayed for calprotectin and potential markers of inflammation, and studied by 16S ribosomal ribonucleic acid (rRNA) gene amplicon sequencing and compared to that of 19 healthy controls and 43 controls with Crohn's disease. Data on intestinal symptoms, diet and quality of life were collected.ResultsPatients with CLD had increased abundances of Proteobacteria, Veillonella, and Prevotella, and lower abundances of normally dominant taxa Ruminococcaceae and Lachnospiraceae when compared with healthy controls and Crohn's disease. No major differences in fecal microbiota were found between CLD and CLD-associated IBD (including two with yet untreated IBD). Butyrate was poorly tolerated and showed no major effects on fecal microbiota or biomarkers in CLD.ConclusionsFecal microbiota in CLD is different from that of healthy subjects or Crohn's disease. Unexpectedly, no changes in the microbiota or fecal markers characterized CLD-associated IBD, an entity with high frequency among patients with CLD.Peer reviewe