Modifying gut integrity and microbiome in children with severe acute malnutrition using legume-based feeds (MIMBLE): A pilot trial

Abstract

Highlights d Inpatient feeding with standard or legume-based feeds resulted in similar weight gain d Legume feeds limited antibiotic-mediated decrease in gut microbiota richness at day 7 d Microbial fermentation was preserved, which has implications for gut health and integrity d Further testing of legume-enriched feeds in severe acute malnutrition is warranted

The synergistic interaction of systemic inflammation, dysbiosis and antimicrobial resistance promotes growth restriction in children with acute severe malnutrition: An emphasis on Escherichia coli

“…A case-control study in Mali compared the feces from 143 malnourished children against 110 healthy children, revealing that M. smithii, was significantly downregulated in stool samples from SAM children even after the administration of therapeutic diet (Camara et al, 2021). An additional Ugandan study reported that dying SAM children had a poor gut microbiota diversity, with a significant presence of Proteobacteria and Enterobacteriaceae, and reduction in the SCFAs-producing Bacteroidetes and Firmicutes, and importantly, the marker of gut inflammation fecal calprotectin was upregulated in these children (Calder et al, 2021). Both inflammation in SAM and intestinal function are regulated by SCFAs.…”

“…Both inflammation in SAM and intestinal function are regulated by SCFAs. Starch and dietary fiber, both of which are not digested in the upper gastrointestinal tract, are anaerobically fermented mainly through glycolysis by resident microbiota in the gut, generating SCFAs (Parada Venegas et al, 2019;Calder et al, 2021). Indeed, SCFAs such as butyrate, acetate and propionate, are secondary products released as by-products of fermentation by healthy microbiota, microorganisms including Lactobacillus reuteri, Faecalibacterium prausnitzii, Bifidobacterium longum, Akkermansia muciniphila, Roseburia spp., and Clostridium cluster XIVa species (Morrison and Preston, 2016;Yan et al, 2016), and among other roles, they improve energy yield, maintain the mucosal integrity in the gut, regulate the colonic pH, prevent the accumulation of potentially pathogenic organisms, and produce vitamins (Calder et al, 2021).…”

“…Starch and dietary fiber, both of which are not digested in the upper gastrointestinal tract, are anaerobically fermented mainly through glycolysis by resident microbiota in the gut, generating SCFAs (Parada Venegas et al, 2019;Calder et al, 2021). Indeed, SCFAs such as butyrate, acetate and propionate, are secondary products released as by-products of fermentation by healthy microbiota, microorganisms including Lactobacillus reuteri, Faecalibacterium prausnitzii, Bifidobacterium longum, Akkermansia muciniphila, Roseburia spp., and Clostridium cluster XIVa species (Morrison and Preston, 2016;Yan et al, 2016), and among other roles, they improve energy yield, maintain the mucosal integrity in the gut, regulate the colonic pH, prevent the accumulation of potentially pathogenic organisms, and produce vitamins (Calder et al, 2021). Particularly, butyrate is an anti-inflammatory lipid that acts as a primary energetic source for the local gastrointestinal epithelial cells (Attia et al, 2016;Parada Venegas et al, 2019), and propionate, the most abundant SCFA, is a specific smooth muscle relaxer and vasodilator acting on mesenteric small arteries to allow blood flow and oxygen into the colon (Calder et al, 2021).…”

“…Indeed, SCFAs such as butyrate, acetate and propionate, are secondary products released as by-products of fermentation by healthy microbiota, microorganisms including Lactobacillus reuteri, Faecalibacterium prausnitzii, Bifidobacterium longum, Akkermansia muciniphila, Roseburia spp., and Clostridium cluster XIVa species (Morrison and Preston, 2016;Yan et al, 2016), and among other roles, they improve energy yield, maintain the mucosal integrity in the gut, regulate the colonic pH, prevent the accumulation of potentially pathogenic organisms, and produce vitamins (Calder et al, 2021). Particularly, butyrate is an anti-inflammatory lipid that acts as a primary energetic source for the local gastrointestinal epithelial cells (Attia et al, 2016;Parada Venegas et al, 2019), and propionate, the most abundant SCFA, is a specific smooth muscle relaxer and vasodilator acting on mesenteric small arteries to allow blood flow and oxygen into the colon (Calder et al, 2021). Moreover, the metabolism of these SCFAs by epithelial cells that internalize them requires the consumption of O 2 , which stabilizes the hypoxia-inducible factor and regulates epithelial gene expression associated with lipid metabolism and with blockade of proliferation in stem cells (Parada Venegas et al, 2019).…”

“…In addition, it has been shown that the gut microbiota composition of SAM children is dramatically different and less diverse from that of children with a normal dietary status (Tidjani Alou et al, 2017). Instead of ensuring a homeostatic microenvironment in the gut, the dysbiotic microbiota not only potentiates the inflammation in affected children, but also dramatically limits the synthesis and absorption of nutrients at the gut coming from the already scarce diet in SAM children, confining their full growth and development in a critical period of their lives (Calder et al, 2021). The whole inflammation-dysbiosis-growth restriction phenomena in SAM children could be attributed in part to the constant ingestion of fecal-polluted water and alimentary products coming from contaminated soil enriched in enteropathogenic bacteria such as Escherichia coli (Odonkor and Mahami, 2020), which are prone to promiscuous horizontal transference of antimicrobial resistant genes (Frazão et al, 2019).…”