Reviews:

Review, 2018: Microbial impact on cholesterol and bile acid metabolism: current status and future prospects http://www.jlr.org/content/early/2018/11/28/jlr.R088989.full.pdf+html

Review, 2018: Nutritional Modulation of Innate Immunity: The Fat–Bile–Gut Connection https://doi.org/10.1016/j.tem.2018.08.002

Review, 2018: Bile acids in glucose metabolism in health and disease: http://jem.rupress.org/content/early/2018/01/12/jem.20171965.long

Review, 2017: Bile acid control of metabolism and inflammation in obesity, type 2 diabetes, dyslipidemia and non-alcoholic fatty liver disease. A review showing how important & multifaceted bile is. Via sci-hub.

Review, 2017: Bile acids at the cross-roads of gut microbiome–host cardiometabolic interactions https://dmsjournal.biomedcentral.com/articles/10.1186/s13098-017-0299-9

Review, 2017: A similar review that includes FXR - Targeting the Gut Microbiota–FXR Signaling Axis for Glycemic Control: Does a Dietary Supplement Work Magic?

Review, 2016: Interaction of gut microbiota with bile acid metabolism and its influence on disease states.

Review, 2017: Bile Acids and the Gut Liver Axis. Disease-Associated Changes in Bile Acid Profiles and Links to Altered Gut Microbiota. Via sci-hub.

Review, 2017: Bile Acids and Intestinal Microbiota in Autoimmune Cholestatic Liver Diseases. "Dysbiosis of the intestinal microbiome can exert profound influence on the bile acid pool and significantly alters the immunological balance of the gut-liver axis in cholestatic liver diseases."

Review, 2017: Interactions between Bacteria and Bile Salts in the Gastrointestinal and Hepatobiliary Tracts: https://www.frontiersin.org/articles/10.3389/fmed.2017.00163/full

Misc:

Fecal transplant success may depend on bile acid metabolism: https://www.medpagetoday.com/meetingcoverage/ddw/65141 - "Inter-individual Recovery Of The Microbiota And Metabolome Over Time Following Fecal Microbiota Transplantation In Patients With Recurrent Clostridium difficile Infection" (2017): http://www.biorxiv.org/content/biorxiv/early/2017/05/24/141846.full.pdf

Altered bile acid profile associates with cognitive impairment in Alzheimer's disease—An emerging role for gut microbiome (Oct 2018): https://doi.org/10.1016/j.jalz.2018.07.217

Bile-mediated dysbiosis as a cause of carcinogenesis: Secondary bile acid‐induced dysbiosis promotes intestinal carcinogenesis (2017): http://onlinelibrary.wiley.com/doi/10.1002/ijc.30643/abstract - It's not directly caused by the bile, but by the dysbiosis the bile (secondary bile acids) causes.

Gallbladder-derived surfactant protein D (delivered to the intestine via bile) regulates gut commensal bacteria for maintaining intestinal homeostasis: http://www.pnas.org/content/early/2017/09/05/1712837114.abstract

Pharmacological Activation of PXR and CAR Down-regulates Distinct Bile Acid-metabolizing Intestinal Bacteria and Alters Bile Acid Homeostasis (2018): https://doi.org/10.1093/toxsci/kfy271

Bile acid is a significant host factor shaping the gut microbiome of diet-induced obese mice (2017): https://bmcbiol.biomedcentral.com/articles/10.1186/s12915-017-0462-7

The gut microbiota drives the impact of bile acids and fat source in diet on mouse metabolism (2018): https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-018-0510-8

Up to 50% of cases of chronic diarrhea/IBS-D is Bile Acid Malabsorption: https://archive.is/HGfvh

Treating mice with antibiotics changes antitumor immune function in the liver due to changes in bile acid metabolism (2018): /r/HumanMicrobiome/comments/8m4fh4 - "one bacterial species, Clostridium scindens, controls metabolism of bile acids in the mouse gut—and ultimately CXCL16 expression, NKT cell accumulation, and tumor growth in the liver"

Gut microbiota bile acid metabolism controls cancer immunosurveillance (2018): https://www.nature.com/articles/s41579-018-0053-9

Bile Acids, the Microbiome, Immunity, and Liver Tumors (2018): https://www.nejm.org/doi/10.1056/NEJMcibr1807106 Bile acids affect the expression of a chemokine ligand by liver sinusoidal endothelial cells, which in turn affects the extent to which a type of natural killer cell is present in and diminishes the burden of hepatocellular carcinomas in a mouse model of the disease.