Yersina perstis interactions with macrophages
Yersina perstis interactions with macrophages
批准号:
11007413
负责人:
Catherine Ayn Brissette
金额:
$22.57万
依托单位国家:
美国
项目类别:
财政年份:
2023
资助国家:
美国
项目状态:
未结题
起止时间:
2023-07-01 至 2026-06-30
中文摘要
鼠疫,一种新出现的传染病,在包括北方在内的多个大陆流行
英文摘要
Plague, an emerging infectious disease endemic to multiple continents, including North
and South America, is a top priority in national biodefense. Studying pathogenic yersiniae, the
bacteria responsible for plague, provides valuable insights into pathogenesis and evolution.
Genomic sequencing of the Yersinia genus and extensive Yersinia pestis genomes spanning
from the Bronze Age to the present offer a rich resource for this research.
A distinct feature of plague infections is the lack of inflammation at bacterial replication
sites. Recent studies on pneumonic plague reveal a two-phase course: a delayed inflammatory
response followed by a highly inflammatory phase as the disease progresses. In the initial
phase, non-human primate and mouse models show no cellular infiltration. Extracellular
presence of Y. pestis in primate lungs does not trigger inflammation. In a rat model of bubonic
plague, neutrophil infiltration into draining lymph nodes is delayed, and infected sites undergo
necrosis instead of inflammation. Comparisons between Y. pseudotuberculosis and Y. pestis
infections demonstrate neutrophil recruitment but inadequate containment of the infection.
Research on the type III secretion system and other virulence factors has explored their role in
neutralizing early inflammatory responses. However, understanding macrophage polarization
during early plague stages remains incomplete. A central hypothesis suggests that Y. pestis
prevents inflammation by inhibiting M1 polarization or inducing M2 macrophages Investigating
these mechanisms will enhance knowledge of how macrophage polarization contributes to early
immune suppression in plague, preventing the infiltration of polymorphonuclear leukocytes
(PMNs) and promoting the initial anti-inflammatory stage of plague.
Aim 1. Investigate macrophage polarization after Yersinia pestis exposure to block
inflammation by either inhibiting M1 polarization or inducing M2 macrophages.
Aim 2. Determine signaling pathways induced and mechanisms used by Y. pestis to
influence macrophage polarization.
Aim 3. Examine the virulence factors utilized by Y. pestis to polarize macrophages.
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会议论文
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批准号:10652565
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资助金额:$41.38万
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负责人:Catherine Ayn Brissette
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依托单位:
Bacterial and host factors in the pathogenesis of Lyme neuroborreliosis
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Role of Borrelia burgdorferi Rev fibronectin binding proteins in Lyme disease
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批准号:8318658
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项目类别:
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资助金额:$10.8万
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财政年份:2011
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依托单位:
Project 3
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批准号:9924574
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项目类别:
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资助金额:$29.25万
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财政年份:--
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负责人:Catherine Ayn Brissette
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依托单位:
Project 3
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批准号:9273570
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项目类别:
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资助金额:$25.11万
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财政年份:--
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负责人:Catherine Ayn Brissette
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依托单位:
Project 3
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批准号:8813008
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项目类别:
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资助金额:$24.99万
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财政年份:--
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负责人:Catherine Ayn Brissette
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依托单位: