Interaction of Host‐Microbial Metabolism in Sepsis

The majority of species of the human gut microbiota is not cultivated on artificial nutrient media, but they are included in the functioning of microbial metabolic conveyor. Between the numerous gut bacteria (transmitter) and billions of intracellular mitochondria (receiver), the function of signaling molecules performs aromatic metabolites. Sepsis destroys the coordinated work of the indigenous anaerobic microflora. This leads to the imbalance of aromatic microbial metabolites (AMM). We hypothesized and proved diagnostic and pathogenic significance of this. First, deficiency of the end products of microbial metabolism—lipophilic AMM (PhPA and derivatives‐cinnamic and benzoic acids) in sepsis, and second, excessive accumulation in blood of intermediate products named, “sepsis‐associated” AMM—both lead to the development of mitochondrial dysfunction. Particularly, the total suppressed production of mROS can manifest by “hibernate‐like state” of cells and lead to MOF. The participation of aromatic metabolites in the development of septic shock can be explained by the inhibition of tyrosine hydroxylase and impaired synthesis of catecholamines. In clinical research, the high levels of “sepsis‐associated” AMM (p‐HPhAA, p‐HPhLA, and PhLA) correlate with the severity according to APACHE II, Sepsis-related Organ Failure Assessments (SOFA) score and mortality. To improve the survival of ICU patients, requires more attention to the role of imbalance of microbial metabolites in sepsis