ena-STUDY-UNIVERSITY OF BRITISH COLUMBIA-20-07-2018-23:47:12:715-599
Stunted childhood growth is associated with decompartmentalization of the gastrointestinal tract and overgrowth of oropharyngeal taxa
Linear growth delay (stunting) affects roughly 155 million children under the age of five worldwide. Treatment has been limited by a lack of understanding of the underlying pathophysiological mechanisms. Stunting is most likely associated with changes in the microbial community of the small intestine, a compartment vital for digestion and nutrient absorption. Efforts to better understand the pathophysiology have been hampered by difficulty of access to small intestinal fluids. Here, we describe for the first time the microbial community found in the upper gastrointestinal tract of stunted children. We studied 46 duodenal and 57 gastric samples from stunted children as well as 404 fecal samples from stunted and non-stunted children aged 2-5 years living in Bangui, Central African Republic and in Antananarivo, Madagascar, using 16S Illumina Amplicon sequencing and semi-quantitative culture methods. The vast majority of the stunted children showed small intestinal bacterial overgrowth dominated by bacteria that normally reside in the oropharyngeal cavity. There was an overrepresentation of oral bacteria in fecal samples of stunted children opening the way for developing non-invasive diagnostic markers. In addition, E. coli/Shigella sp. and Campylobacter sp. were found to be more prevalent in stunted children, while Clostridia, well-known butyrate producers, were reduced. Our data suggest that stunting is associated with a microbiome “decompartmentalization” of the gastrointestinal tract characterized by an increased presence of oropharyngeal bacteria from the stomach to the colon, hence challenging the current view of stunting arising solely as a consequence of small intestine overstimulation through recurrent infections by enteric pathogens.
Linear growth delay (stunting) affects roughly 155 million children under the age of five worldwide. Treatment has been limited by a lack of understanding of the underlying pathophysiological mechanisms. Stunting is most likely associated with changes in the microbial community of the small intestine, a compartment vital for digestion and nutrient absorption. Efforts to better understand the pathophysiology have been hampered by difficulty of access to small intestinal fluids. Here, we describe for the first time the microbial community found in the upper gastrointestinal tract of stunted children. We studied 46 duodenal and 57 gastric samples from stunted children as well as 404 fecal samples from stunted and non-stunted children aged 2-5 years living in Bangui, Central African Republic and in Antananarivo, Madagascar, using 16S Illumina Amplicon sequencing and semi-quantitative culture methods. The vast majority of the stunted children showed small intestinal bacterial overgrowth dominated by bacteria that normally reside in the oropharyngeal cavity. There was an overrepresentation of oral bacteria in fecal samples of stunted children opening the way for developing non-invasive diagnostic markers. In addition, E. coli/Shigella sp. and Campylobacter sp. were found to be more prevalent in stunted children, while Clostridia, well-known butyrate producers, were reduced. Our data suggest that stunting is associated with a microbiome “decompartmentalization” of the gastrointestinal tract characterized by an increased presence of oropharyngeal bacteria from the stomach to the colon, hence challenging the current view of stunting arising solely as a consequence of small intestine overstimulation through recurrent infections by enteric pathogens.