2017 Fiscal Year Final Research Report
Innate immunity reaction in marcophage for periprosthetic joint infection
| Project/Area Number |
15K10459
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Yamagata University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
佐々木 幹 山形大学, 医学部, 非常勤講師 (00444034)
高窪 祐弥 山形大学, 医学部, 准教授 (80431641)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | 人工関節 / インプラント感染症 |
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| Outline of Final Research Achievements |
One of big problems is periprosthetic joint infection (PJI) in total joint arthroplasty. PJI cause a severe loosening of implant. Innate immunity and its effector mechanism with immune sensors, Toll-like receptor (TLR) and Nod-like receptor (NLR) at the forefront of host defense. We’ve reported the presenting of several TLRs and NLRs in macrophages of septic granuloma. We summarized TLRs and NLRs in septic THA. When TLRs recognized abnormal antigens, they stimulate production of proinflammatory cytokines and inflammasome.
Innate sensors including TLRs or NLRs were well-equipped in each subset of macrophage in septic loosening tissues around artificial hip joint in different manner depending on the pathologic conditions.
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| Free Research Field |
整形外科学
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