Loading…

L‐lactate promotes intestinal epithelial cell migration to inhibit colitis

Lactate, one of the most common primary metabolites of bacteria and human cells, has been shown to play essential roles in the regulation of inflammatory diseases, including inflammatory bowel diseases. However, whether and how host‐derived lactate affects intestinal epithelial homeostasis is still...

Full description

Saved in:
Bibliographic Details
Published in:The FASEB journal 2021-04, Vol.35 (4), p.e21554-n/a
Main Authors: Yu, Yu, Yang, Wenjing, Bilotta, Anthony J., Zhao, Xiaojing, Cong, Yingzi, Li, Yanqing
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Lactate, one of the most common primary metabolites of bacteria and human cells, has been shown to play essential roles in the regulation of inflammatory diseases, including inflammatory bowel diseases. However, whether and how host‐derived lactate affects intestinal epithelial homeostasis is still not completely understood. Here, we investigated how L‐lactate, mainly produced by host cells, regulates intestinal epithelial cell (IEC) migration to promote intestinal wound healing. Using video microscopy and tracking individual cells, we found that L‐lactate enhanced IEC migration in direction persistence and speed. Mechanistically, L‐lactate promoted IEC mitochondrial ATP production. The mitochondrial ATP synthase inhibitor, oligomycin, significantly decreased IEC persistence and speed, which inhibited cell migration induced by L‐lactate. Furthermore, administering mice with L‐lactate suppressed colitis induced by dextran sulfate sodium. In conclusion, our study demonstrates that host‐derived L‐lactate promotes IEC mitochondrial ATP production to drive cell migration, promoting intestinal wound healing to alleviate intestinal inflammation.
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.202100095R