Lipocalin 2 inhibits the expressions of interleukin-8 and macrophage inflammatory protein-1α in human neutrophil-like cells

IF 2.3 Q1 DENTISTRY, ORAL SURGERY & MEDICINE

Journal of Oral Biosciences Pub Date : 2025-02-01 DOI:10.1016/j.job.2025.100624

Rie Kido , Yuka Hiroshima , Jun-ichi Kido , Mika Bando , Kaya Yoshida , Yuji Inagaki , Hiromichi Yumoto

{"title":"Lipocalin 2 inhibits the expressions of interleukin-8 and macrophage inflammatory protein-1α in human neutrophil-like cells","authors":"Rie Kido , Yuka Hiroshima , Jun-ichi Kido , Mika Bando , Kaya Yoshida , Yuji Inagaki , Hiromichi Yumoto","doi":"10.1016/j.job.2025.100624","DOIUrl":null,"url":null,"abstract":"<div><h3>Objectives</h3><div>Lipocalin 2 (LCN2) is a glycoprotein with multiple functions, including antimicrobial activity, inflammatory response modulation, and cell migration. LCN2 is expressed in some cells, such as epithelial cells and neutrophils, and its levels are increased in inflammatory diseases. This study investigated the presence of LCN2 receptor (24p3R) in cells around periodontal tissues and function of LCN2 in cells with a receptor to explore the role of LCN2 in periodontal diseases.</div></div><div><h3>Methods</h3><div>The presence of 24p3R was examined in periodontal cells, including human gingival fibroblasts, periodontal ligament fibroblasts, human oral epithelial cells (HOECs), and neutrophil-like cells (HL-60), by Western blotting. Changes in periodontal disease-associated proteins in the presence of recombinant LCN2 (rLCN2) were examined using a protein array in differentiated HL-60 (dHL-60) cells. Interleukin-8 (IL-8) and macrophage inflammatory protein-1α (MIP-1α) mRNA expressions were analyzed by qRT-PCR, and IL-8 and MIP-1α levels in dHL-60 cells treated with rLCN2 or <em>Porphyromonas gingivalis</em>-lipopolysaccaharide (<em>P.g</em>-LPS) were determined by enzyme-linked immunosorbent assay.</div></div><div><h3>Results</h3><div>We detected 24p3R in dHL-60 cells. IL-8 was highly expressed and MIP-1α was weakly expressed in dHL-60 cells using a protein array. rLCN2 significantly decreased IL-8 mRNA and protein levels and suppressed <em>P.g</em>-LPS-induced IL-8 production in dHL-60 cells. As dHL-60 cells were co-cultured with HOECs in which LCN2 was knocked down, IL-8 mRNA expression increased in dHL-60 cells. Furthermore, rLCN2 inhibited MIP-1α production in dHL-60 cells.</div></div><div><h3>Conclusion</h3><div>LCN2 suppresses inflammatory responses by regulating IL-8 and MIP-1α expression in periodontal diseases.</div></div>","PeriodicalId":45851,"journal":{"name":"Journal of Oral Biosciences","volume":"67 1","pages":"Article 100624"},"PeriodicalIF":2.3000,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Oral Biosciences","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1349007925000131","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"DENTISTRY, ORAL SURGERY & MEDICINE","Score":null,"Total":0}

引用次数: 0

Abstract

Objectives

Lipocalin 2 (LCN2) is a glycoprotein with multiple functions, including antimicrobial activity, inflammatory response modulation, and cell migration. LCN2 is expressed in some cells, such as epithelial cells and neutrophils, and its levels are increased in inflammatory diseases. This study investigated the presence of LCN2 receptor (24p3R) in cells around periodontal tissues and function of LCN2 in cells with a receptor to explore the role of LCN2 in periodontal diseases.

Methods

The presence of 24p3R was examined in periodontal cells, including human gingival fibroblasts, periodontal ligament fibroblasts, human oral epithelial cells (HOECs), and neutrophil-like cells (HL-60), by Western blotting. Changes in periodontal disease-associated proteins in the presence of recombinant LCN2 (rLCN2) were examined using a protein array in differentiated HL-60 (dHL-60) cells. Interleukin-8 (IL-8) and macrophage inflammatory protein-1α (MIP-1α) mRNA expressions were analyzed by qRT-PCR, and IL-8 and MIP-1α levels in dHL-60 cells treated with rLCN2 or Porphyromonas gingivalis-lipopolysaccaharide (P.g-LPS) were determined by enzyme-linked immunosorbent assay.

Results

We detected 24p3R in dHL-60 cells. IL-8 was highly expressed and MIP-1α was weakly expressed in dHL-60 cells using a protein array. rLCN2 significantly decreased IL-8 mRNA and protein levels and suppressed P.g-LPS-induced IL-8 production in dHL-60 cells. As dHL-60 cells were co-cultured with HOECs in which LCN2 was knocked down, IL-8 mRNA expression increased in dHL-60 cells. Furthermore, rLCN2 inhibited MIP-1α production in dHL-60 cells.

Conclusion

LCN2 suppresses inflammatory responses by regulating IL-8 and MIP-1α expression in periodontal diseases.

查看原文本刊更多论文

Lipocalin 2抑制人中性粒细胞样细胞中白细胞介素-8和巨噬细胞炎症蛋白-1α的表达。

目的：脂载蛋白2 （Lipocalin 2, LCN2）是一种具有多种功能的糖蛋白，包括抗菌活性、炎症反应调节和细胞迁移。LCN2在一些细胞中表达，如上皮细胞和中性粒细胞，其水平在炎症性疾病中升高。本研究通过研究LCN2受体（24p3R）在牙周组织周围细胞中的存在以及LCN2在具有受体的细胞中的功能，探讨LCN2在牙周疾病中的作用。方法：采用Western blotting法检测人牙龈成纤维细胞、牙周韧带成纤维细胞、人口腔上皮细胞（HOECs）、嗜中性粒细胞样细胞（HL-60）等牙周细胞中24p3R的表达。在分化的HL-60 （dHL-60）细胞中使用蛋白质阵列检测重组LCN2 （rLCN2）存在时牙周病相关蛋白的变化。采用qRT-PCR分析白细胞介素-8 （IL-8）和巨噬细胞炎症蛋白-1α (MIP-1α) mRNA的表达，采用酶联免疫吸附法检测rLCN2或牙龈卟啉单胞菌-脂多糖（P.g-LPS）处理的dHL-60细胞中IL-8和MIP-1α的水平。结果：dHL-60细胞中检测到24p3R。在dHL-60细胞中，IL-8高表达，MIP-1α弱表达。rLCN2显著降低IL-8 mRNA和蛋白水平，抑制p.g - lps诱导的dHL-60细胞IL-8的产生。将dHL-60细胞与敲除LCN2的HOECs共培养后，IL-8 mRNA在dHL-60细胞中表达升高。此外，rLCN2抑制dHL-60细胞中MIP-1α的产生。结论：LCN2通过调节牙周病组织中IL-8和MIP-1α的表达来抑制炎症反应。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊