The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation
Bacterial infections of bones remain a serious complication of endoprosthetic surgery. These infections are difficult to treat, because many bacterial species form biofilms on implants, which are relatively resistant towards antibiotics. Bacterial biofilms elicit a progressive local inflammatory res...
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Wiley
2014-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2014/728619 |
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author | Ulrike Dapunt Susanne Maurer Thomas Giese Matthias Martin Gaida Gertrud Maria Hänsch |
author_facet | Ulrike Dapunt Susanne Maurer Thomas Giese Matthias Martin Gaida Gertrud Maria Hänsch |
author_sort | Ulrike Dapunt |
collection | DOAJ |
description | Bacterial infections of bones remain a serious complication of endoprosthetic surgery. These infections are difficult to treat, because many bacterial species form biofilms on implants, which are relatively resistant towards antibiotics. Bacterial biofilms elicit a progressive local inflammatory response, resulting in tissue damage and bone degradation. In the majority of patients, replacement of the prosthesis is required. To address the question of how the local inflammatory response is linked to bone degradation, tissue samples were taken during surgery and gene expression of the macrophage inflammatory proteins MIP1α (CCL3) and MIP2α (CXCL2) was assessed by quantitative RT-PCR. MIPs were expressed predominantly at osteolytic sites, in close correlation with CD14 which was used as marker for monocytes/macrophages. Colocalisation of MIPs with monocytic cells could be confirmed by histology. In vitro experiments revealed that, aside from monocytic cells, also osteoblasts were capable of MIP production when stimulated with bacteria; moreover, CCL3 induced the differentiation of monocytes to osteoclasts. In conclusion, the multifunctional chemokines CCL3 and CXCL2 are produced locally in response to bacterial infection of bones. In addition to their well described chemokine activity, these cytokines can induce generation of bone resorbing osteoclasts, thus providing a link between bacterial infection and osteolysis. |
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id | doaj-art-15ea6d64781b4c94b1aa081e1a978edd |
institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2014-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-15ea6d64781b4c94b1aa081e1a978edd2025-02-03T05:59:27ZengWileyMediators of Inflammation0962-93511466-18612014-01-01201410.1155/2014/728619728619The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone DegradationUlrike Dapunt0Susanne Maurer1Thomas Giese2Matthias Martin Gaida3Gertrud Maria Hänsch4Department of Orthopaedics and Trauma Surgery, University Hospital Heidelberg, Schlierbacher Landstraße 200a, 69118 Heidelberg, GermanyDepartment of Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120 Heidelberg, GermanyDepartment of Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120 Heidelberg, GermanyDepartment of Pathology, Heidelberg University, Im Neuenheimer Feld 224, 69120 Heidelberg, GermanyDepartment of Immunology, Heidelberg University, Im Neuenheimer Feld 305, 69120 Heidelberg, GermanyBacterial infections of bones remain a serious complication of endoprosthetic surgery. These infections are difficult to treat, because many bacterial species form biofilms on implants, which are relatively resistant towards antibiotics. Bacterial biofilms elicit a progressive local inflammatory response, resulting in tissue damage and bone degradation. In the majority of patients, replacement of the prosthesis is required. To address the question of how the local inflammatory response is linked to bone degradation, tissue samples were taken during surgery and gene expression of the macrophage inflammatory proteins MIP1α (CCL3) and MIP2α (CXCL2) was assessed by quantitative RT-PCR. MIPs were expressed predominantly at osteolytic sites, in close correlation with CD14 which was used as marker for monocytes/macrophages. Colocalisation of MIPs with monocytic cells could be confirmed by histology. In vitro experiments revealed that, aside from monocytic cells, also osteoblasts were capable of MIP production when stimulated with bacteria; moreover, CCL3 induced the differentiation of monocytes to osteoclasts. In conclusion, the multifunctional chemokines CCL3 and CXCL2 are produced locally in response to bacterial infection of bones. In addition to their well described chemokine activity, these cytokines can induce generation of bone resorbing osteoclasts, thus providing a link between bacterial infection and osteolysis.http://dx.doi.org/10.1155/2014/728619 |
spellingShingle | Ulrike Dapunt Susanne Maurer Thomas Giese Matthias Martin Gaida Gertrud Maria Hänsch The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation Mediators of Inflammation |
title | The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation |
title_full | The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation |
title_fullStr | The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation |
title_full_unstemmed | The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation |
title_short | The Macrophage Inflammatory Proteins MIP1α (CCL3) and MIP2α (CXCL2) in Implant-Associated Osteomyelitis: Linking Inflammation to Bone Degradation |
title_sort | macrophage inflammatory proteins mip1α ccl3 and mip2α cxcl2 in implant associated osteomyelitis linking inflammation to bone degradation |
url | http://dx.doi.org/10.1155/2014/728619 |
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