Treatment of periodontitis by homing M2 macrophages
归巢M2巨噬细胞治疗牙周炎
基本信息
- 批准号:9296130
- 负责人:
- 金额:$ 23.05万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2016
- 资助国家:美国
- 起止时间:2016-07-01 至 2020-06-30
- 项目状态:已结题
- 来源:
- 关键词:AddressAdultAffectAlveolar Bone LossAnti-Inflammatory AgentsAnti-inflammatoryBacteriaBacterial InfectionsBehaviorBiologicalBiological AssayBirthCCL17 geneCCL2 geneCCL22 geneCalculiCanis familiarisCardiovascular DiseasesCellsChemotaxisChronicClinical TreatmentControl GroupsDataDebridementDental CalculusDental PlaqueDental cariesDiabetes MellitusDiseaseDisease modelEnzyme-Linked Immunosorbent AssayGingival PocketGlycolatesHomingImmuneImmune responseImmunohistochemistryImpaired wound healingIn VitroInbred BALB C MiceInfiltrationInflammationInflammatoryInflammatory ResponseInjectableInterleukin-10Interleukin-13Interleukin-4IntestinesLaboratoriesLymphocyteMethodsMicrobeModelingMorphologyMouth DiseasesMusOutcome StudyPeriodontal DiseasesPeriodontal PocketPeriodontitisPhenotypePlayPopulationPropertyPublic HealthRecombinantsRecruitment ActivityRegulatory T-LymphocyteResearchResolutionRoleRoot ScalingSignal Recognition ParticleSiteSystemic diseaseTechniquesTechnologyTestingTherapeuticTissuesTooth LossTopical AntibioticTransforming Growth Factor betaTranslatingUnited StatesX-Ray Computed Tomographyagedalveolar bonebone losschemokinecytokineimmunoregulationin vivomacrophagemonocytemouse modelnew therapeutic targetpathogenresponsestandard caretooth surfacetreatment strategy
项目摘要
PROJECT SUMMARY
Periodontitis is the second most common oral disease, affecting about half of adults (65 millions) in the United
States. Periodontitis causes tooth loss and has been implicated in several serious systemic diseases include
diabetes, cardiovascular diseases, and immature birth. Periodontitis is a chronic inflammatory disease,
triggered by bacterial infection present in dental plaques and calculus, but the disease itself is caused by host
immune response to these pathogens. Current standard treatment is debridement of plaques and calculus to
reduce the bacterial load, however, there are no therapies to address the immune aspect of the diseases.
Thus, many research groups have started developing technologies to regulate the immune response and
reduce inflammation. Our group has focused so far on recruiting T regulatory immune cells new target for
therapy of periodontitis.
In the previous study, we have successfully reduced alveolar bone loss by recruiting regulatory T cells in
mouse and dog periodontitis model. Regulatory T cells were recruited by injecting C-C motif chemokine 22
(CCL22) releasing PLGA microparticles in the periodontal pockets. These results indicated that recruiting
regulatory immune cells by local delivery of chemokine indeed reduces inflammation and bone loss in
periodontitis.
To further explore the principle of “recruitment of regulatory immune cells” and to continue our efforts to
develop better therapies, we hypothesize that recruiting a larger population of anti-inflammatory immune cells
such as M2 macrophages will achieve a better therapeutic option. Macrophages plays an important role in
inflammatory responses, and interestingly have a polarization property by differentiating into M1 (pro-
inflammatory) or M2 (anti-inflammatory) macrophages. Our hypothesis that is strongly supported by our recent
in vivo pilot data is that the local delivery of CCL2 will induce homing of M2 macrophages, and
differentiation of macrophages and monocytes to an M2 phenotype leading to decreased inflammation
and bone loss in periodontal tissue. To test this hypothesis, we set the following specific aims; 1) To
fabricate CCL2 releasing microparticles and analyze recruitment of M2 macrophage and differentiation of
macrophages and monocytes to M2 macrophages and 2) To analyze effect of CCL2 on periodontitis in mouse
model.
We anticipate that CCL2 released from PLGA microparticles will recruit and induce M2 macrophages, and
reduce inflammation and bone loss of periodontal tissue in mouse periodontitis model. Moreover, this concept
could be applied to therapies for other inflammatory diseases such as delayed wound healing of diabetes or
bowel disease.
项目总结
项目成果
期刊论文数量(1)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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CHARLES SFEIR其他文献
CHARLES SFEIR的其他文献
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{{ truncateString('CHARLES SFEIR', 18)}}的其他基金
Pittsburgh Craniofacial Sciences Training Program
匹兹堡颅面科学培训计划
- 批准号:
10657807 - 财政年份:2022
- 资助金额:
$ 23.05万 - 项目类别:
Pittsburgh Craniofacial Sciences Training Program
匹兹堡颅面科学培训计划
- 批准号:
10657803 - 财政年份:2022
- 资助金额:
$ 23.05万 - 项目类别:
Pittsburgh Craniofacial Sciences Training Program
匹兹堡颅面科学培训计划
- 批准号:
10625702 - 财政年份:2022
- 资助金额:
$ 23.05万 - 项目类别:
Treatment of Periodontitis by Homing M2 Macrophages
归巢 M2 巨噬细胞治疗牙周炎
- 批准号:
10649608 - 财政年份:2020
- 资助金额:
$ 23.05万 - 项目类别:
Treatment of Periodontitis by Homing M2 Macrophages
归巢 M2 巨噬细胞治疗牙周炎
- 批准号:
10197100 - 财政年份:2020
- 资助金额:
$ 23.05万 - 项目类别:
Treatment of Periodontitis by Homing M2 Macrophages
归巢 M2 巨噬细胞治疗牙周炎
- 批准号:
10437804 - 财政年份:2020
- 资助金额:
$ 23.05万 - 项目类别:
New Faculty for Craniofacial Tissue Engineering and Biology
颅面组织工程和生物学新教师
- 批准号:
7858926 - 财政年份:2009
- 资助金额:
$ 23.05万 - 项目类别:
New Faculty for Craniofacial Tissue Engineering and Biology
颅面组织工程和生物学新教师
- 批准号:
7934057 - 财政年份:2009
- 资助金额:
$ 23.05万 - 项目类别:
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