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Related Experiment Video

Updated: Mar 10, 2026

Investigation of Macrophage Polarization Using Bone Marrow Derived Macrophages
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Lactylation-Driven Macrophage Polarisation Regulates Pulp Inflammation.

Ziting Wang1,2, Wanli Xu1,2, Tingyun Xu1,2

  • 1Shenzhen Clinical College of Stomatology, School of Stomatology, Southern Medical University, Shenzhen, Guangdong, China.

International Endodontic Journal
|March 9, 2026
PubMed
Summary
This summary is machine-generated.

Elevated lactate in pulpitis drives macrophage reprogramming via lactylation, promoting healing. This study reveals lactate

Keywords:
immunotherapyinflammationinnate immunityposttranslational modificationpulp biologypulpitis

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Area of Science:

  • Immunometabolism
  • Dental Pulp Inflammation
  • Cellular Signaling

Background:

  • Pulpitis involves an inflammatory microenvironment.
  • Lactate accumulation is observed in pulpitis.
  • Macrophage polarization plays a key role in inflammation and repair.

Purpose of the Study:

  • Investigate lactate-induced lactylation in pulpitis.
  • Elucidate the mechanism of immunometabolic crosstalk.
  • Explore the role of lactylation in macrophage polarization and pulp repair.

Main Methods:

  • Quantified lactate levels and lactylation markers (Pan-Kla).
  • Utilized in vitro (THP-1 macrophages, iCM) and in vivo (murine pulpitis model) systems.
  • Performed transcriptomic profiling, metabolic flux assays (OCR/ECAR), and immunofluorescence staining.

Main Results:

  • Elevated lactate and lactylation correlated with M2 macrophage infiltration in pulpitis.
  • In vitro, M1 macrophages upregulated lactylation and shifted to M2-like phenotype upon lactate uptake.
  • Metabolic reprogramming from glycolysis to oxidative phosphorylation was observed, linked to M2 polarization.
  • iCM treatment reduced pro-inflammatory IL-6 and increased anti-inflammatory CD206.

Conclusions:

  • Lactate acts as a mediator in pulpitis, facilitating immunometabolic crosstalk between dental pulp cells and macrophages.
  • Lactylation-induced metabolic reprogramming is a key mechanism.
  • Findings support understanding pulp repair potential and biologically-based preservation strategies.