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Author Spotlight: Enhancing Dental Pulp Research with Improved Mouse Models
Published on: October 27, 2023
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LIF Aggravates Pulpitis by Promoting Inflammatory Response in Macrophages
Donghua Guo1, Wei Dong1, Yaqi Cong1
1State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, 430079, China.
Inflammation
|October 2, 2023
Summary
Leukemia inhibitory factor (LIF) worsens dental pulp inflammation by boosting macrophage responses via a STAT3/p65 pathway. LIF also increases macrophage recruitment to inflamed pulp tissue.
Area of Science:
- Oral Biology
- Immunology
- Inflammation Research
Background:
- Leukemia inhibitory factor (LIF) is an emerging inflammatory modulator.
- Its role in dental pulp inflammation remains largely unexplored.
Purpose of the Study:
- To investigate the role of LIF in dental pulp inflammation.
- To elucidate the mechanisms by which LIF modulates macrophage inflammatory responses.
Main Methods:
- Experimental pulpitis was induced in wild-type and Lif-deficient mice.
- Macrophage inflammatory and chemotaxis responses were assessed in vitro using cell lines and primary cells.
- LIF's effect on inflammatory pathways (STAT3/p65) was examined.
Main Results:
- LIF expression increased with pulpitis progression, with high LIF receptor (LIFR) expression on macrophages.
- Lif deficiency reduced pulpitis severity, pro-inflammatory cytokines, and macrophage infiltration.
- Exogenous LIF exacerbated LPS-induced macrophage inflammation via STAT3/p65.
- LIF-treated dental pulp cells promoted macrophage migration.
Conclusions:
- LIF exacerbates dental pulp inflammation by enhancing macrophage inflammatory responses through a STAT3/p65-dependent pathway.
- LIF is critical for recruiting macrophages to inflamed pulp tissue by influencing chemokine secretion from dental pulp cells.
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