Auto-antibodies as predictive markers for Post treatment Lyme Disease Syndrome
自身抗体作为治疗后莱姆病综合征的预测标记
基本信息
- 批准号:10737996
- 负责人:
- 金额:$ 55.52万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2023
- 资助国家:美国
- 起止时间:2023-07-05 至 2028-06-30
- 项目状态:未结题
- 来源:
- 关键词:AffinityAftercareAnimal ModelAnimalsAntibiotic TherapyAntibodiesAnticardiolipin AntibodiesAntigen-Antibody ComplexAntigensAntiphospholipid AntibodiesAreaArthralgiaAutoantibodiesAutoimmuneAutoimmune DiseasesAutoimmune ProcessAutoimmunityBacteriaBacterial ProteinsBindingBorrelia burgdorferiCardiolipinsCellsCommunicable DiseasesComplement ActivationDefectDepositionDevelopmentDiagnostic testsDiseaseElementsEnvironmentFatigueFibromyalgiaGenerationsGenomeHumanHypersensitivityImmune responseImmune systemImmunoglobulin GImmunologic StimulationInfectionInjectionsLaboratoriesLinkLipidsLocomotionLong COVIDLyme DiseaseMacrophageMembraneMemory B-LymphocyteMemory LossMetabolicModelingMusMyalgiaNerve BlockNeurologicNeuronsNutrientOrganismPainPathogenesisPathogenicityPatientsPersonsPhospholipidsPlasminPost Treatment Lyme Disease SyndromeProcessProductionReaginsReceptor ActivationResidual stateResolutionRoleSerumSignal TransductionSymptomsSynaptic TransmissionSyphilisTestingTheftTimeTissuesacute infectionautoreactivitybehavioral studybiomarker identificationbrain tissuecell injurycostcross reactivityderepressionfibromyalgia patientshistological studieslyme pathogenesisneuralpathogenic autoantibodiespatient subsetspersistent symptompredictive markerresponsetreatment response
项目摘要
ABSTRACT
As an organism that persists in its natural hosts for long periods of time, Borrelia burgdorferi, the causative
agent of Lyme disease, has adapted many strategies for survival and evasion of host immune responses. It
has a very small genome and is unable to produce many essential nutrients for itself and is instead, dependent
upon utilizing them from its environment. We have recently shown that B. burgdorferi is able to acquire host
phospholipids and deploy them, intact, in its membrane. A cost of utilizing host phospholipids is that it may
result in production, or de-repression of autoantibodies to host phospholipid targets. Indeed, in our preliminary
studies, we found that mice and humans infected with B. burgdorferi produce antibodies to host phospholipids
that the organism itself does not produce. Antibodies to phospholipids arise quicker than other antibodies to B.
burgdorferi and also appear to resolve more quickly, as might be expected since autoantibody production is
typically tightly regulated. However, in patients with PTLDS as compared with patients who resolve their
symptoms after treatment for Lyme, there appears to be increased levels of anti-phospholipid antibodies. It is
unknown whether these antibodies may be pathogenic or are just a marker for PTLDS.
In this proposal, we will explore the development of anti-lipid/phospholipid antibodies during Lyme disease and
their potential role in PTLDS. In Aim 1, we will determine the extent of anti-lipid/phospholipid development at
different stages of disease and determine their relationship to disease resolution/persistent symptoms in
patients with Lyme disease. In Aim 2, we will examine binding of these antibodies to human cells and tissues
and look for the presence of immune complexes which are often deposited in auto-immune diseases. Finally,
in Aim 3, we will explore a new animal model for PTLDS. A recent study has shown that injection of antibodies
from patients with fibromyalgia, a disease with marked similarities to PTLDS in symptoms, into mice results in
hypersensitivity to pain and cold as well as changes in locomotion. Histological studies have shown binding of
the human antibodies to neural tissues and macrophages. We will test a similar model using serum from
patients with PTLDS, recovered Lyme disease and fibromyalgia. In our preliminary studies, we have found
increased binding of antibodies from PTLDS patients to mouse brain tissue compared with binding from
healthy control antibodies. The discovery of autoantibodies to lipids/phospholipids opens a new area for
discovery in the pathogenesis for Lyme disease and may lead to better diagnostic tests and a new
understanding of the pathogenesis of this disease.
摘要
项目成果
期刊论文数量(0)
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Linden T Hu其他文献
Case 24-2015
案例24-2015
- DOI:
- 发表时间:
2015 - 期刊:
- 影响因子:0
- 作者:
Linden T Hu;Athe M. N. Tsibris;John A. Branda - 通讯作者:
John A. Branda
Linden T Hu的其他文献
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{{ truncateString('Linden T Hu', 18)}}的其他基金
Laboratory for Combinatorial Drug Regimen Design for Resistant and Emerging Pathogens
耐药和新发病原体组合药物方案设计实验室
- 批准号:
10596722 - 财政年份:2022
- 资助金额:
$ 55.52万 - 项目类别:
Role of human innate immune mutations in loss of tolerance to Borrelia burgdorferi
人类先天免疫突变在伯氏疏螺旋体耐受性丧失中的作用
- 批准号:
10461854 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Development and Field Testing of a Novel Reservoir Targeted Antibiotic Against Borrelia burgdorferi
新型水库靶向伯氏疏螺旋体抗生素的开发和现场测试
- 批准号:
10397615 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Role of human innate immune mutations in loss of tolerance to Borrelia burgdorferi
人类先天免疫突变在伯氏疏螺旋体耐受性丧失中的作用
- 批准号:
10680556 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Development and Field Testing of a Novel Reservoir Targeted Antibiotic Against Borrelia burgdorferi
新型水库靶向伯氏疏螺旋体抗生素的开发和现场测试
- 批准号:
10606624 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Development and Field Testing of a Novel Reservoir Targeted Antibiotic Against Borrelia burgdorferi
新型水库靶向伯氏疏螺旋体抗生素的开发和现场测试
- 批准号:
10165497 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Role of human innate immune mutations in loss of tolerance to Borrelia burgdorferi
人类先天免疫突变在伯氏疏螺旋体耐受性丧失中的作用
- 批准号:
10256713 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Development and Field Testing of a Novel Reservoir Targeted Antibiotic Against Borrelia burgdorferi
新型水库靶向伯氏疏螺旋体抗生素的开发和现场测试
- 批准号:
10674121 - 财政年份:2020
- 资助金额:
$ 55.52万 - 项目类别:
Understanding Human Immunological Responses to Ixodes Tick Bites
了解人类对硬蜱叮咬的免疫反应
- 批准号:
9807836 - 财政年份:2019
- 资助金额:
$ 55.52万 - 项目类别:
Coping with Stress: Next Generation Approaches to Borrelia burgdorferi Host Adaptation
应对压力:伯氏疏螺旋体宿主适应的下一代方法
- 批准号:
9892949 - 财政年份:2017
- 资助金额:
$ 55.52万 - 项目类别:
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