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L‐lactate promotes intestinal epithelial cell migration to inhibit colitis
Author(s) -
Yu Yu,
Yang Wenjing,
Bilotta Anthony J.,
Zhao Xiaojing,
Cong Yingzi,
Li Yanqing
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202100095r
Subject(s) - oligomycin , colitis , cell migration , microbiology and biotechnology , lactic acid , atp synthase , cell , inflammation , glycolysis , intestinal mucosa , homeostasis , chemistry , mitochondrion , wound healing , biology , biochemistry , immunology , metabolism , bacteria , medicine , atpase , enzyme , genetics
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.