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Article: LIF Aggravates Pulpitis by Promoting Inflammatory Response in Macrophages

TitleLIF Aggravates Pulpitis by Promoting Inflammatory Response in Macrophages
Authors
KeywordsInflammation
Leukemia inhibitory factor
Macrophage
Pulpitis
Issue Date2-Oct-2023
PublisherSpringer
Citation
Inflammation, 2023 How to Cite?
Abstract

Leukemia inhibitory factor (LIF) has been recognized as a novel inflammatory modulator in inflammation-associated diseases. This study aimed to investigate the modulation of LIF in dental pulp inflammation. Experimental pulpitis was established in wild-type (WT) and Lif-deficient (Lif−/−) mice. Histological and immunostaining analyses were conducted to assess the role of LIF in the progression of pulpitis. Mouse macrophage cell line (RAW264.7) was treated with LPS to simulate an inflammatory environment. Exogenous LIF was added to this system to examine its modulation in macrophage inflammatory response in vitro. Primary bone marrow-derived macrophages (BMDMs) from WT and Lif−/− mice were isolated and stimulated with LPS to confirm the effect of Lif deletion on macrophage inflammatory response. Supernatants from LIF and LPS-treated human dental pulp cells (hDPCs) were collected and added to macrophages. Macrophage chemotaxis was assessed using transwell assays. The results showed an increased expression of LIF and LIFR with the progression of pulpitis, and LIFR was highly expressed in macrophages. Lif deficiency alleviated experimental pulpitis with the reduction of pro-inflammatory cytokines and macrophage infiltration. Exogenous LIF promoted inflammatory response of LPS-induced macrophages through a STAT3/p65-dependent pathway. Consistently, Lif deletion inhibited macrophage inflammatory response in vitro. Supernatants of LIF-treated hDPCs enhanced macrophage migration in LPS-induced inflammatory environment. Our findings demonstrated that LIF aggravates pulpitis by promoting macrophage inflammatory response through a STAT3/p65-dependent pathway. Furthermore, LIF plays a crucial role in driving the recruitment of macrophages to inflamed pulp tissue by promoting chemokine secretion in DPCs.


Persistent Identifierhttp://hdl.handle.net/10722/339205
ISSN
2021 Impact Factor: 4.657
2020 SCImago Journal Rankings: 1.027
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGuo, Donghua-
dc.contributor.authorDong, Wei-
dc.contributor.authorCong, Yaqi-
dc.contributor.authorLiu, Yi-
dc.contributor.authorLiang, Youde-
dc.contributor.authorYe, Zhou-
dc.contributor.authorZhang, Jiali-
dc.contributor.authorZhou, Yi -
dc.date.accessioned2024-03-11T10:34:48Z-
dc.date.available2024-03-11T10:34:48Z-
dc.date.issued2023-10-02-
dc.identifier.citationInflammation, 2023-
dc.identifier.issn0360-3997-
dc.identifier.urihttp://hdl.handle.net/10722/339205-
dc.description.abstract<p>Leukemia inhibitory factor (LIF) has been recognized as a novel inflammatory modulator in inflammation-associated diseases. This study aimed to investigate the modulation of LIF in dental pulp inflammation. Experimental pulpitis was established in wild-type (WT) and <em>Lif</em>-deficient (<em>Lif</em><sup><em>−/−</em></sup>) mice. Histological and immunostaining analyses were conducted to assess the role of LIF in the progression of pulpitis. Mouse macrophage cell line (RAW264.7) was treated with LPS to simulate an inflammatory environment. Exogenous LIF was added to this system to examine its modulation in macrophage inflammatory response <em>in vitro</em>. Primary bone marrow-derived macrophages (BMDMs) from WT and <em>Lif</em><sup><em>−/−</em></sup> mice were isolated and stimulated with LPS to confirm the effect of <em>Lif</em> deletion on macrophage inflammatory response. Supernatants from LIF and LPS-treated human dental pulp cells (hDPCs) were collected and added to macrophages. Macrophage chemotaxis was assessed using transwell assays. The results showed an increased expression of LIF and LIFR with the progression of pulpitis, and LIFR was highly expressed in macrophages. <em>Lif</em> deficiency alleviated experimental pulpitis with the reduction of pro-inflammatory cytokines and macrophage infiltration. Exogenous LIF promoted inflammatory response of LPS-induced macrophages through a STAT3/p65-dependent pathway. Consistently, <em>Lif</em> deletion inhibited macrophage inflammatory response <em>in vitro</em>. Supernatants of LIF-treated hDPCs enhanced macrophage migration in LPS-induced inflammatory environment. Our findings demonstrated that LIF aggravates pulpitis by promoting macrophage inflammatory response through a STAT3/p65-dependent pathway. Furthermore, LIF plays a crucial role in driving the recruitment of macrophages to inflamed pulp tissue by promoting chemokine secretion in DPCs.<br></p>-
dc.languageeng-
dc.publisherSpringer-
dc.relation.ispartofInflammation-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectInflammation-
dc.subjectLeukemia inhibitory factor-
dc.subjectMacrophage-
dc.subjectPulpitis-
dc.titleLIF Aggravates Pulpitis by Promoting Inflammatory Response in Macrophages-
dc.typeArticle-
dc.identifier.doi10.1007/s10753-023-01910-6-
dc.identifier.scopuseid_2-s2.0-85173077971-
dc.identifier.eissn1573-2576-
dc.identifier.isiWOS:001073667400001-
dc.identifier.issnl0360-3997-

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