Young children with cystic fibrosis (CF) exhibit a more pro-inflammatorygastrointestinal microbiome, which may underlie impaired nutrient absorption, according to the study “Metagenomic evidence for taxonomic dysbiosis and functional imbalance in the gastrointestinal tracts of children with cystic fibrosis,” published in the journal Scientific Reports. The results suggest that therapeutics modulating the intestinal microbiome in these children may improve their health and fat absorption.Patients with CF, a genetic disorder characterized by the buildup of thick, sticky mucus that can damage several organs, often develop inflammation and gastrointestinal problems, including poor digestion and absorption of nutrients (particularly proteins, fats, and fat-soluble vitamins), and gastrointestinal obstruction. The disease is caused by the loss or dysfunction of activity in the cystic fibrosis transmembrane conductance regulator (CFTR) channel as a result of mutations in the Cftr gene.

The role of the microbiome in health is increasingly being recognized in the scientific community; however, the link between microbiome composition and the digestive manifestations associated with CF remains largely unaddressed.

The authors performed a metagenomics analysis of fecal samples from children with and without CF to systematically characterize their microbiome, and determine whether a link could be detected between CF-associated dysbiosis, inflammation, and fat content.

Researchers found that dysbiosis (i.e., an unbalance in the natural, healthy bacteria in the gut, with reduced levels of essential bacteria) is more predominant in CF children, particularly at young ages and diminishing with time. Most importantly, they found that the dysbiotic microbiomes of CF children had an impact on metabolic functions. Specifically, significant alterations were found in lipid metabolism, including impaired capacity for overall fatty acid biosynthesis and increased capacity for degrading anti-inflammatory short-chain fatty acids. These alterations correlated with CF fat malabsorption and gut inflammation.

In conclusion, results showed that the fecal microbiome of children with CF is markedly different from those without the disease as a result of high abundance of unabsorbed luminal fatty acid. Impaired absorption of fat, in essence, promotes a pro-inflammatory gastrointestinal microbiome in young children with the disease. Future research is necessary to investigate how the manipulation of the microbiome might improve outcomes for these children.

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