. 2022 May 12;12(5):723. doi: 10.3390/life12050723

Table 3.

Consequences of gut dysbiosis.

Types of Dysbiosis	Consequences
Storage of an abnormal substrate in the intestinal lumen (undigested nutrients, medications) [32]. Disruption of proper microbiome function caused by lack of commensal bacteria (C. hiranonis) [47]. Increase in the total number of bacteria, primarily in the small intestine [32]. Increased mucosa- adherent bacteria [32].	Increase in bacterial species, causing osmotic/secretory diarrhoea (conversion of fatty acids to hydroxystearic acids, metabolites of mycophenolate motefil) [32]. Bacterial overgrowth (C. difficile, C. perfringens, E. coli) caused by lack of conversion from primary to secondary BAs. Lack of anti-inflammatory microbial-derived metabolites [63]. Increased production of microbial metabolites leading to osmotic/secretory diarrhoea. Activation of inflammatory reactions [32]. Increased adhesion of bacteria to the intestinal mucosa causes increased inflammatory reactions [32].

Types of Dysbiosis

Consequences

Storage of an abnormal substrate in the intestinal lumen (undigested nutrients, medications) [32].
Disruption of proper microbiome function caused by lack of commensal bacteria (C. hiranonis) [47].
Increase in the total number of bacteria, primarily in the small intestine [32].
Increased mucosa- adherent bacteria [32].

Increase in bacterial species, causing osmotic/secretory diarrhoea (conversion of fatty acids to hydroxystearic acids, metabolites of mycophenolate motefil) [32].
Bacterial overgrowth (C. difficile, C. perfringens, E. coli) caused by lack of conversion from primary to secondary BAs.

Lack of anti-inflammatory microbial-derived metabolites [63].
Increased production of microbial metabolites leading to osmotic/secretory diarrhoea.

Activation of inflammatory reactions [32].
Increased adhesion of bacteria to the intestinal mucosa causes increased inflammatory reactions [32].