Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis

IntroductionOsseous echinococcosis, caused by Echinococcus granulosus infection, is characterized by progressive bone destruction driven by abnormal osteoclast activation. Dual-specificity phosphatase 4 (DUSP4), a key negative regulator of the MAPK pathway, inhibits osteoclast differentiation and bo...

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Main Authors: Haohao Sun, Yaqing Liu, Yiping Huang, Kangjun Xiong, Zhendong Zhang, Weishan Wang, Yi Dai, Jing Li, Qi Li, Sibo Wang, Chenhui Shi
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-03-01
Series:Frontiers in Microbiology
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Online Access:https://www.frontiersin.org/articles/10.3389/fmicb.2025.1558603/full
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author Haohao Sun
Yaqing Liu
Yaqing Liu
Yiping Huang
Kangjun Xiong
Zhendong Zhang
Weishan Wang
Yi Dai
Jing Li
Qi Li
Sibo Wang
Chenhui Shi
author_facet Haohao Sun
Yaqing Liu
Yaqing Liu
Yiping Huang
Kangjun Xiong
Zhendong Zhang
Weishan Wang
Yi Dai
Jing Li
Qi Li
Sibo Wang
Chenhui Shi
author_sort Haohao Sun
collection DOAJ
description IntroductionOsseous echinococcosis, caused by Echinococcus granulosus infection, is characterized by progressive bone destruction driven by abnormal osteoclast activation. Dual-specificity phosphatase 4 (DUSP4), a key negative regulator of the MAPK pathway, inhibits osteoclast differentiation and bone resorption. This study aimed to elucidate the role of DUSP4 in E. granulosus-induced bone loss.MethodsIn vitro, a co-culture system of E. granulosus protoscoleces (PSCs) and bone marrow-derived macrophages (BMMs) was established. Osteoclast differentiation and bone resorption were assessed using TRAP staining and F-actin immunofluorescence. Transcriptome sequencing identified DUSP4 as a key regulator. DUSP4 overexpression was performed to evaluate its effects on osteoclast markers and MAPK signaling (ERK, JNK, p38). In vivo, a mouse model of osseous echinococcosis was developed, and DUSP4 overexpression was achieved via lentiviral transduction. Bone destruction was analyzed using X-ray, micro-CT, and histology.ResultsPSCs significantly enhanced osteoclast differentiation and bone resorption, upregulated osteoclast markers (CTSK, NFATc1), and activated MAPK signaling. DUSP4 overexpression reversed these effects, reducing osteoclast activity and MAPK phosphorylation. In vivo, PSC infection caused severe bone destruction, which was mitigated by DUSP4 overexpression.DisscussionThis study reveals the molecular mechanism by which Echinococcus granulosus drives abnormal osteoclast activation through the DUSP4-MAPK signaling axis. Parasitic infection suppresses DUSP4 expression, relieving its negative regulation of the MAPK pathway and leading to excessive osteoclast differentiation. Restoring DUSP4 expression effectively reverses abnormal MAPK pathway activation, reducing osteoclast bone resorption activity to physiological levels. These findings not only provide new insights into the pathological mechanisms of bone destruction in osseous echinococcosis but also establish DUSP4 as a critical therapeutic target for pathological bone resorption, laying the groundwork for host-directed treatment strategies for parasitic bone diseases.
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spelling doaj-art-cce4c6eb281649f2bff24bf8f98670b32025-08-20T02:06:46ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2025-03-011610.3389/fmicb.2025.15586031558603Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosisHaohao Sun0Yaqing Liu1Yaqing Liu2Yiping Huang3Kangjun Xiong4Zhendong Zhang5Weishan Wang6Yi Dai7Jing Li8Qi Li9Sibo Wang10Chenhui Shi11The First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe Medical College of Shihezi University, Shihezi, ChinaThe Medical College of Shihezi University, Shihezi, ChinaThe Medical College of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaXi’an Jiaotong University Affiliated Honghui Hospital, Xi’an, ChinaThe First Affiliated Hospital of Shihezi University, Shihezi, ChinaIntroductionOsseous echinococcosis, caused by Echinococcus granulosus infection, is characterized by progressive bone destruction driven by abnormal osteoclast activation. Dual-specificity phosphatase 4 (DUSP4), a key negative regulator of the MAPK pathway, inhibits osteoclast differentiation and bone resorption. This study aimed to elucidate the role of DUSP4 in E. granulosus-induced bone loss.MethodsIn vitro, a co-culture system of E. granulosus protoscoleces (PSCs) and bone marrow-derived macrophages (BMMs) was established. Osteoclast differentiation and bone resorption were assessed using TRAP staining and F-actin immunofluorescence. Transcriptome sequencing identified DUSP4 as a key regulator. DUSP4 overexpression was performed to evaluate its effects on osteoclast markers and MAPK signaling (ERK, JNK, p38). In vivo, a mouse model of osseous echinococcosis was developed, and DUSP4 overexpression was achieved via lentiviral transduction. Bone destruction was analyzed using X-ray, micro-CT, and histology.ResultsPSCs significantly enhanced osteoclast differentiation and bone resorption, upregulated osteoclast markers (CTSK, NFATc1), and activated MAPK signaling. DUSP4 overexpression reversed these effects, reducing osteoclast activity and MAPK phosphorylation. In vivo, PSC infection caused severe bone destruction, which was mitigated by DUSP4 overexpression.DisscussionThis study reveals the molecular mechanism by which Echinococcus granulosus drives abnormal osteoclast activation through the DUSP4-MAPK signaling axis. Parasitic infection suppresses DUSP4 expression, relieving its negative regulation of the MAPK pathway and leading to excessive osteoclast differentiation. Restoring DUSP4 expression effectively reverses abnormal MAPK pathway activation, reducing osteoclast bone resorption activity to physiological levels. These findings not only provide new insights into the pathological mechanisms of bone destruction in osseous echinococcosis but also establish DUSP4 as a critical therapeutic target for pathological bone resorption, laying the groundwork for host-directed treatment strategies for parasitic bone diseases.https://www.frontiersin.org/articles/10.3389/fmicb.2025.1558603/fullEchinococcus granulosus (E. granulosus)boneosteoclastDUSP4MAPK
spellingShingle Haohao Sun
Yaqing Liu
Yaqing Liu
Yiping Huang
Kangjun Xiong
Zhendong Zhang
Weishan Wang
Yi Dai
Jing Li
Qi Li
Sibo Wang
Chenhui Shi
Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
Frontiers in Microbiology
Echinococcus granulosus (E. granulosus)
bone
osteoclast
DUSP4
MAPK
title Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
title_full Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
title_fullStr Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
title_full_unstemmed Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
title_short Echinococcus granulosus sensu lato promotes osteoclast differentiation through DUSP4-MAPK signaling in osseous echinococcosis
title_sort echinococcus granulosus sensu lato promotes osteoclast differentiation through dusp4 mapk signaling in osseous echinococcosis
topic Echinococcus granulosus (E. granulosus)
bone
osteoclast
DUSP4
MAPK
url https://www.frontiersin.org/articles/10.3389/fmicb.2025.1558603/full
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