Study type: In vivo/preclinical · Status: Verified against declared source
Modulating intestinal neuroimmune VIPergic signaling attenuates the reduction in ILC3-derived IL-22 and hepatic steatosis in MASLD.
Hepatology communications · 2024
Study scale: Despite previous descriptions of the effects of IL-22 on lipid metabolism, the exact mechanism by which IL-22 could modulate MASLD progression is not fully understood.
Abstract only: Open source record
Product or molecular entity relationships
- VIP: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.
Plain-language verified summary
Question
Metabolic dysfunction–associated steatotic liver disease (MASLD, formerly known as NAFLD) describes a spectrum of diseases ranging from liver steatosis to liver inflammation, liver fibrosis, and end-stage cirrhosis.
Methods
Under homeostasis, type 3 innate lymphoid cells (ILC3) are one of the main producers of IL-22 in the intestine.20 We recently identified in mice a neuroimmune circuit that downregulates IL-22 production by intestinal ILC3 during feeding but not during fasting.18 This neuroimmune circuit is formed by the interaction between vasoactive intestinal peptide (VIP)-producing neurons and ILC3.
Scale or participants
Despite previous descriptions of the effects of IL-22 on lipid metabolism, the exact mechanism by which IL-22 could modulate MASLD progression is not fully understood.
Key findings
Production of IL-22 by intestinal ILC3 is reduced in steatotic mice that were exposed to an HFD for 16 weeks.
Limitations and uncertainty
Metabolic dysfunction–associated steatotic liver disease (MASLD, formerly known as NAFLD) is a major driver of cirrhosis and liver-related mortality.
Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.