The microbiota-derived bile acid taurodeoxycholic acid improves hepatic cholesterol levels in mice with cancer cachexia.

Alterations in bile acid profile and pathways contribute to hepatic inflammation in cancer cachexia, a syndrome worsening the prognosis of cancer patients. As the gut microbiota impinges on host metabolism through bile acids, the current study aimed to explore the functional contribution of gut microbial dysbiosis to bile acid dysmetabolism and associated disorders in cancer cachexia. Using three mouse models of cancer cachexia (the C26, MC38 and HCT116 models), we evidenced a reduction in the hepatic levels of several secondary bile acids, mainly taurodeoxycholic (TDCA).

New discoveries in bile acids, gut microbiota and host interactions in health and diseases.

Over the past 20 years, basic research has robustly demonstrated the regulatory role of bile acids in physiological processes, primarily by the discovery and the study of their specific receptors and the understanding of the pathways they modulate. The dysregulation of the bile acid pool and the perturbation of bile acid signaling have been implicated in the pathophysiology of various clinical conditions, including cardiometabolic, cholestatic and inflammatory diseases. Consequently, bile acids have emerged as promising therapeutic targets, with compounds to modulate bile acid metabolism and signaling being actively investigated in pre-clinical and clinical settings.

Interleukin 38 reduces antigen-presentation capacity and antibody production after vaccination.

The mechanisms that underpin low vaccine responses, which can lead to inadequate protection against infection, are still partially unclear. Interleukin (IL)-38 is a member of the IL-1 family, expressed by B cells among others, that regulates inflammatory responses. A recent study shows that IL-38 suppresses plasma cell generation and antibody production upon immune activation.