# Ace Deficiency Induces Intestinal Inflammation in Zebrafish

## TL;DR

This study shows that a deficiency in the ace gene causes intestinal inflammation in zebrafish, offering new insights into inflammatory bowel disease.

## Contribution

The study identifies ace as a novel gene involved in intestinal inflammation and IBD pathogenesis in zebrafish.

## Key findings

- Ace deletion in zebrafish increases inflammatory marker gene expression in the intestine.
- Ace−/− mutants show higher mucus secretion and are more susceptible to DSS-induced enteritis.
- Ace plays a critical role in maintaining intestinal homeostasis.

## Abstract

Inflammatory bowel disease (IBD) is a nonspecific chronic inflammatory disease resulting from an immune disorder in the intestine that is prone to relapse and incurable. The understanding of the pathogenesis of IBD remains unclear. In this study, we found that ace (angiotensin-converting enzyme), expressed abundantly in the intestine, plays an important role in IBD. The deletion of ace in zebrafish caused intestinal inflammation with increased expression of the inflammatory marker genes interleukin 1 beta (il1b), matrix metallopeptidase 9 (mmp9), myeloid-specific peroxidase (mpx), leukocyte cell-derived chemotaxin-2-like (lect2l), and chemokine (C-X-C motif) ligand 8b (cxcl8b). Moreover, the secretion of mucus in the ace−/− mutants was significantly higher than that in the wild-type zebrafish, validating the phenotype of intestinal inflammation. This was further confirmed by the IBD model constructed using dextran sodium sulfate (DSS), in which the mutant zebrafish had a higher susceptibility to enteritis. Our study reveals the role of ace in intestinal homeostasis, providing a new target for potential therapeutic interventions.