Restricting these bacteria requires IL-18 and failure promotes CCL5-dependent colonic inflammation and increased TLR4 and TLR9 agonist influx into the portal vein, which eventually causes non-alcoholic fatty liver disease (NAFLD), a comorbidity associated with obesity, metabolic syndrome, and NASH progression (144, 230). Here, CCL5 is linked to metabolic dysfunction-associated steatotic liver disease.