These methanogens contribute to an average human body methane emission of about 0.35 l per day, released through the breath and flatus. smithii, Methanosphaera stadtmanae) and Methanomassiliicoccales ( Ca. In the human GIT, methanogens are mainly represented by the Methanobacteriales ( M. By consuming by-products of bacterial metabolism (H 2, CO 2, formate, methyl-compounds, acetate), they particularly contribute to keeping the hydrogen concentration low, which would inhibit the fermentation activity and reduce the overall energy yield. By maintaining numerous syntrophic relationships with bacteria, methanogens control the efficiency of the bacterial primary and secondary fermentation of complex organic molecules. The role of methanogens per se in health and disease is not yet clear, and analyses suffer from methodological pitfalls to correctly detect and characterize the human archaeome as well as the contradictory information that appears in the literature (reviewed in ).Īlthough the average abundance of archaea in human fecal samples is low as compared to bacteria, methanogens are considered to represent key-stone species in the GIT. Although not a single pathogenic archaeal representative has been identified, human-associated archaea are widespread in the GIT as well as other body sites (e.g. Methane-forming archaea (‘methanogens’) in the gastrointestinal tract (GIT) were first observed long ago-through the detection of methane in the human breath and flatus (see also ). While its role as a gasotransmitter is controversially discussed, methane is causally linked to a slowed gastrointestinal motility (transit time slowed down by up to 59%), probably caused by the direct action of methane on the cholinergic pathway of the enteric nervous system. Although methane is not utilized by the human itself, elevated methane levels, measured in breath, have been linked with small intestinal bacterial overgrowth, colorectal cancer, diverticulosis and other gastrointestinal disorders (summarized in ).
Methane is the metabolic end-product of a non-bacterial sub-population of the gastrointestinal microbiome, namely the archaeome. This study enlightens the complex, multi-level interplay of host diet, genetics and microbiome composition/function leading to two fundamentally different gastrointestinal phenotypes and identifies novel points of therapeutic action in methane-associated disorders.
These metabolites were strongly correlated with dietary habits, such as vitamin, fat and fibre intake, and microbiome function, altogether driving archaeal methanogenesis. As confirmed by metagenomics and metabolomics, the biology of high methane producers was further characterized by increased formate and acetate levels in the gut. This archaeon co-occurred with a bacterial community specialized on dietary fibre degradation, which included members of Ruminococcaceae and Christensenellaceae. The microbiomes of high methane emitters were characterized by a 1000-fold increase in Methanobrevibacter smithii. On the basis of the amount of methane emitted, participants were grouped into high methane emitters (CH 4 breath content 5–75 ppm) and low emitters (CH 4 < 5 ppm). We assessed the breath methane content, the gastrointestinal microbiome, its function and metabolome, and dietary intake of one-hundred healthy young adults (female: n = 52, male: n = 48 mean age =24.1).
The underlying principle for differential methane emission and its effect on human health is not sufficiently understood. Twenty percent of the (healthy) Western populations innately exhale substantially higher amounts (>5 ppm) of this gas. Increased methane production has been associated with abdominal pain, bloating, constipation, IBD, CRC or other conditions. This gas is solely produced by an archaeal subpopulation of the human microbiome. Methane is an end product of microbial fermentation in the human gastrointestinal tract.
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