Bile acid detergency: permeability, inflammation, and effects of sulfation.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic biochemistry and preclinical data without original clinical trial data or systematic methodology
PubMed 35258349 · doi:10.1152/ajpgi.00011.2022
What was done
This narrative review examined the concentrations of bile acids entering the human colon in physiological and pathological states, the molecular determinants of detergent function (focusing on di-alpha-hydroxy bile acids), their role in mucosal bacterial uptake, mucin depletion, and epithelial damage, and the influence of bile salt sulfation on colonic inflammation.
What was found
Bile acids reach the human colon at concentrations of 2 to 10 mM. Di-alpha-hydroxy bile acids specifically exert detergent actions leading to mucin depletion, mucosal damage, bacterial uptake, and low-grade inflammation in conditions such as bile acid diarrhea, neuroendocrine tumors, ileal resection, and nonalcoholic steatohepatitis. Sulfation prevents colonic secretion induced by primary bile acids but may render secondary bile acids proinflammatory; preclinical models further link reduced sulfation to barrier breakdown, inflammation, and carcinogenesis.
Why it matters
It clarifies the biochemical and structural mechanisms by which unabsorbed bile acid species disrupt colonic epithelial integrity and drive mucosal inflammation across gastrointestinal and metabolic disorders.
Limits
This is an unsystematic narrative review lacking study selection criteria, sample sizes, or quantitative meta-analysis. Several underlying mechanisms, particularly regarding sulfation and carcinogenesis, are derived from preclinical animal or in vitro models rather than direct human trials.
Cited by
- supports Excessive accumulation of secondary bile salts, produced when gut microbes convert primary bile, can cause inflammation in the large intestine.