It is generally believed that the infant's microbiota is established during the first 1–2 years of life. However, there is scarce data on its characterization and its comparison to the adult-like microbiota in consecutive years. To characterize and compare the intestinal microbiota in healthy young children (1–4 years) and healthy adults from the North Carolina region in the U.S. using high-throughput bacterial phylogenetic microarray analysis. Detailed characterization and comparison of the intestinal microbiota of healthy children aged 1–4 years old (n = 28) and healthy adults of 21–60 years (n = 23) was carried out using the Human Intestinal Tract Chip (HITChip) phylogenetic microarray targeting the V1 and V6 regions of 16S rRNA and quantitative PCR. The HITChip microarray data indicate that Actinobacteria, Bacilli, Clostridium cluster IV and Bacteroidetes are the predominant phylum-like groups that exhibit differences between young children and adults. The phylum-like group Clostridium cluster XIVa was equally predominant in young children and adults and is thus considered to be established at an early age. The genus-like level show significant 3.6 fold (higher or lower) differences in the abundance of 26 genera between young children and adults. Young U.S. children have a significantly 3.5-fold higher abundance of Bifidobacterium species than the adults from the same location. However, the microbiota of young children is less diverse than that of adults. We show that the establishment of an adult-like intestinal microbiota occurs at a later age than previously reported. Characterizing the microbiota and its development in the early years of life may help identify ‘windows of opportunity’ for interventional strategies that may promote health and prevent or mitigate disease processes.

The colonization pattern of intestinal microbiota during childhood may impact health later in life, but children older than 1 year are poorly studied. We followed healthy children aged 1–4 years (n=28) for up to 12 months, during which a synbiotic intervention and occasional antibiotics intake occurred, and compared them with adults from the same region. Microbiota was quantified with the HITChip phylogenetic microarray and analyzed with linear mixed effects model and other statistical approaches. Synbiotic administration increased the stability of Actinobacteria and antibiotics decreased Clostridium cluster XIVa abundance. Bacterial diversity did not increase in 1- to 5-year-old children and remained significantly lower than in adults. Actinobacteria, Bacilli and Clostridium cluster IV retained child-like abundances, whereas some other groups were converting to adult-like profiles. Microbiota stability increased, with Bacteroidetes being the main contributor. The common core of microbiota in children increased with age from 18 to 25 highly abundant genus-level taxa, including several butyrate-producing organisms, and developed toward an adult-like composition. In conclusion, intestinal microbiota is not established before 5 years of age and diversity, core microbiota and different taxa are still developing toward adult-type configuration. Discordant development patterns of bacterial phyla may reflect physiological development steps in children.

Background: Celiac disease (CD) is an autoimmune disorder of the small intestine which is triggered by dietary gluten in genetically predisposed (HLA-DQ2/DQ8 positive) individuals. Only a fraction of HLA-DQ2/DQ8 positive individuals develop CD indicating that other factors have a role in the disorder. Several studies have addressed intestinal microbiota aberrancies in pediatric CD, but the results are inconsistent. Previously, we demonstrated that pediatric CD patients have lower duodenal expression of TLR2 and higher expression of TLR9 as compared to healthy controls (HC) indicating that microbiota may have a role in CD. Methods: We used bacterial phylogenetic microarray to comprehensively profile the microbiota in duodenal biopsies of CD (n = 10) and HC (n = 9) children. The expression of selected mucosa-associated genes was assessed by qRT-PCR in CD and HC children and in treated CD adults (T-CD, n = 6) on gluten free diet. Results: The overall composition, diversity and the estimated microbe associated molecular pattern (MAMP) content of microbiota were comparable between CD and HC, but a sub-population profile comprising eight genus-like bacterial groups was found to differ significantly between HC and CD. In HC, increased TLR2 expression was positively correlated with the expression of tight junction protein ZO-1. In CD and T-CD, the expression of IL-10, IFN-g and CXCR6 were higher as co5mpared to HC. Conclusions: The results suggest that microbiota and altered expression of mucosal receptors have a role in CD. In CD subjects, the increased expression of IL-10 and IFN-g may have partly resulted from the increased TLR9 expression and signaling.

Optimal gut motility is central to bowel function and gut health. The link between the gut dysmotility related disorders and dysfunctional-intestinal barriers has led to a hypothesis that certain probiotics could help in normalizing gut motility and maintain gut health. This review investigates the roles of Bifidobacterium animalis subsp. lactis HN019 (B. lactis HN019™) on gut health, and its mechanisms of action in various pre-clinical and clinical studies. Research supports the hypothesis that B. lactis HN019™ has a beneficial role in maintaining intestinal barrier function during gastrointestinal infections by competing and excluding potential pathogens via different mechanisms; maintaining normal tight junction function in vitro; and regulating host immune defense toward pathogens in both in vitro and human studies. This has been observed to lead to reduced incidence of diarrhea. Interestingly, B. lactis HN019™ also supports normal physiological function in immunosenescent elderly and competes and excludes potential pathogens. Furthermore, B. lactis HN019™ reduced intestinal transit time and increased bowel movement frequency in functional constipation, potentially by modulating gut–brain–microbiota axis, mainly via serotonin signaling pathway, through short chain fatty acids derived from microbial fermentation. B. lactis HN019™ is thus a probiotic that can contribute to relieving gut dysmotility related disorders.

Probiotic is little known for its benefits on upper gastrointestinal health. The objective of this systematic review was to examine the efficacy of probiotics in alleviating the frequency and severity of symptoms in gastroesophageal reflux disease (GERD) in the general adult population. The PubMed and Web of Science databases were searched for prospective studies on GERD, heartburn, regurgitation, and dyspepsia, without any limitation on sample size. The Jadad scale was used to evaluate the quality of randomized controlled trials. In total, 13 prospective studies that were published in 12 articles were included in the analysis and scored per the Jadad scale as high- (five studies), medium- (two), and low- (six) quality. One article reported on two probiotic groups; thus, 14 comparisons were included in the selected studies, of which 11 (79%) reported positive benefits of probiotics on symptoms of GERD. Five out of 11 positive outcomes (45%) noted benefits on reflux symptoms: three noted reduced regurgitation; improvements in reflux or heartburn were seen in one study; five (45%) saw improvements in dyspepsia symptoms; and nine (81%) saw improvements in other upper gastrointestinal symptoms, such as nausea (three studies), abdominal pain (five), and gas-related symptoms (four), such as belching, gurgling, and burping. In conclusion, probiotic use can be beneficial for GERD symptoms, such as regurgitation and heartburn. However, proper placebo-controlled, randomized, and double-blinded clinical trials with a sufficient number of participants are warranted to confirm its efficacy in alleviating these symptoms. Further, interventions with longer durations and an intermediate analysis of endpoints should be considered to determine the proper therapeutic window.

Inflammatory bowel diseases (IBD), ulcerative colitis (UC) and Crohn’s disease (CD), are chronic debilitating disorders of unknown etiology. Over 200 genetic risk loci are associated with IBD, highlighting a key role for immunological and epithelial barrier functions. Environmental factors account for the growing incidence of IBD, and microbiota are considered as an important contributor. Microbiota dysbiosis can lead to a loss of tolerogenic immune effects and initiate or exacerbate inflammation. We aimed to study colonic mucosal microbiota and the expression of selected host genes in pediatric UC. We used high-throughput 16S rDNA sequencing to profile microbiota in colonic biopsies of pediatric UC patients (n = 26) and non-IBD controls (n = 27). The expression of 13 genes, including five for antimicrobial peptides, in parallel biopsies was assessed with qRT-PCR. The composition of microbiota between UC and non-IBD differed significantly (PCoA, p = 0.001). UC children had a decrease in Bacteroidetes and an increase in several family-level taxa including Peptostreptococcaceae and Enterobacteriaceae, which correlated negatively with the expression of antimicrobial peptides REG3G and DEFB1, respectively. Enterobacteriaceae correlated positively with the expression siderophore binding protein LCN2 and Betaproteobacteria negatively with DEFB4A expression. The results indicate that reciprocal interaction of epithelial microbiota and defense mechanisms play a role in UC.