Investigating the role of the pattern recognition receptor Nod2 in delayed wound healing in the elderly

研究模式识别受体Nod2在老年人伤口愈合延迟中的作用

基本信息

  • 批准号:
    G1000449/1
  • 负责人:
  • 金额:
    $ 52.13万
  • 依托单位:
  • 依托单位国家:
    英国
  • 项目类别:
    Research Grant
  • 财政年份:
    2011
  • 资助国家:
    英国
  • 起止时间:
    2011 至 无数据
  • 项目状态:
    已结题

项目摘要

Approximately, one in twenty elderly people develop skin wounds that do not heal resulting in significant pain, distress and even death. These non-healing wounds are also at risk of becoming infected by harmful bacteria (pathogens). The body recognizes bacteria via specialized receptors called pattern recognition receptors (PRRs). These will respond to pathogens and trigger an immune response to kill the pathogen. However, the skin is covered in ?friendly bacteria? that may, as has been shown in the gut, be beneficial for wound healing. Ideally immune responses to bacteria should be tightly controlled so that the immune cells destroy the pathogens whilst ignoring the friendly bacteria. If the immune responses are not properly regulated there can be serious consequences including an inappropriate negative reaction to friendly bacteria. One way to maintain this balance is by down-regulating PRR function in response to specific bacteria, an event controlled by the PRR, Nod2 and others. Importantly, altered Nod2 function has been linked to chronic inflammation in both the gut and skin. We also have shown that Nod2 and other PRRs are reduced in elderly humans. This suggests that in the skin of older people the immune responses to bacteria are altered. We have observed that mice lacking Nod2 are unable to effectively heal skin wounds and in this respect resemble elderly humans. We believe that Nod2 is critical for normal wound healing and that its reduced function in the elderly delays wound healing, perhaps via altered immune responses to bacteria. At present there are few effective treatments for chronic delayed healing with most focusing on addressing the symptoms rather than prevention e.g. maggots used to remove dead tissue. As we are an aging population, there is an urgent need to understand why skin healing is delayed in the elderly, which will then allow us to develop better treatments. Successful completion of this project will reveal the role of Nod2, and interaction with bacteria, in delayed skin wound healing. Improved understanding of this crucial area will lead to the development of better treatments for chronic skin wounds.
大约每二十个老年人中就有一个会出现无法愈合的皮肤伤口,导致严重的疼痛、痛苦甚至死亡。这些不愈合的伤口也有被有害细菌(病原体)感染的风险。身体通过称为模式识别受体(PRR)的特殊受体识别细菌。这些将对病原体作出反应,并引发免疫反应以杀死病原体。然而,皮肤是覆盖在?友好的细菌?正如在肠道中所显示的那样,这可能有利于伤口愈合。理想情况下,对细菌的免疫反应应该受到严格控制,这样免疫细胞就可以摧毁病原体,而忽略友好的细菌。如果免疫反应没有得到适当的调节,可能会产生严重的后果,包括对友好细菌的不适当的负面反应。维持这种平衡的一种方法是通过下调PRR功能来响应特定的细菌,这是由PRR,Nod2等控制的事件。重要的是,Nod2功能的改变与肠道和皮肤的慢性炎症有关。我们还表明,Nod2和其他PRR在老年人中减少。这表明,在老年人的皮肤中,对细菌的免疫反应发生了变化。我们已经观察到,缺乏Nod2的小鼠无法有效地愈合皮肤伤口,在这方面类似于老年人。我们认为Nod2对正常伤口愈合至关重要,其在老年人中的功能降低可能会延迟伤口愈合,这可能是通过改变对细菌的免疫反应。目前,对慢性延迟愈合的有效治疗方法很少,大多数集中在解决症状而不是预防,例如用于去除死亡组织的蛆。由于我们是一个老龄化的人口,迫切需要了解为什么老年人的皮肤愈合延迟,这将使我们能够开发更好的治疗方法。该项目的成功完成将揭示Nod2在延迟皮肤伤口愈合中的作用以及与细菌的相互作用。对这一关键领域的进一步了解将有助于开发更好的慢性皮肤伤口治疗方法。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

Matthew Hardman其他文献

Seismic Vulnerability Analysis of Bridges in Mountainous States
山地桥梁地震易损性分析
  • DOI:
  • 发表时间:
    2013
  • 期刊:
  • 影响因子:
    0
  • 作者:
    Matthew Hardman;Thomas Wilson;Suren Chen
  • 通讯作者:
    Suren Chen

Matthew Hardman的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('Matthew Hardman', 18)}}的其他基金

MICA: The role of arginase in chronic delayed wound healing
MICA:精氨酸酶在慢性伤口愈合延迟中的作用
  • 批准号:
    MR/L010267/2
  • 财政年份:
    2016
  • 资助金额:
    $ 52.13万
  • 项目类别:
    Research Grant
MICA: The role of arginase in chronic delayed wound healing
MICA:精氨酸酶在慢性伤口愈合延迟中的作用
  • 批准号:
    MR/L010267/1
  • 财政年份:
    2014
  • 资助金额:
    $ 52.13万
  • 项目类别:
    Research Grant
The role of PCKalpha and modulation of desmosomal adhesion in delayed wound healing in the elderly
PCKα 和桥粒粘附调节在老年人伤口愈合延迟中的作用
  • 批准号:
    G0800004/1
  • 财政年份:
    2008
  • 资助金额:
    $ 52.13万
  • 项目类别:
    Research Grant

相似国自然基金

PfAP2-R介导的PfCRT转录调控在恶性疟原虫对喹啉类药物抗性中的作用及机制研究
  • 批准号:
    82372275
  • 批准年份:
    2023
  • 资助金额:
    49.00 万元
  • 项目类别:
    面上项目
Sestrin2抑制内质网应激对早产儿视网膜病变的调控作用及其机制研究
  • 批准号:
    82371070
  • 批准年份:
    2023
  • 资助金额:
    49.00 万元
  • 项目类别:
    面上项目

相似海外基金

Investigating the relationship between Sympathetic Nervous System Development and Neuroblastoma
研究交感神经系统发育与神经母细胞瘤之间的关系
  • 批准号:
    10658015
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating relationships between naturalistic light exposure and sleep
研究自然光照与睡眠之间的关系
  • 批准号:
    10739430
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating non-canonical mechanisms of endogenous opioids on motivation in dorsal midbrain
研究内源性阿片类药物对背侧中脑动机的非典型机制
  • 批准号:
    10624699
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating tonic and synaptic excitatory signaling in the bed nucleus of the stria terminalis across models of alcohol exposure
研究酒精暴露模型中终纹床核的强直和突触兴奋信号传导
  • 批准号:
    10825889
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating a rare pediatric enteropathy caused by ADAM17 loss of function using iPSC-derived human intestinal organoids
使用 iPSC 衍生的人肠道类器官研究由 ADAM17 功能丧失引起的罕见儿童肠病
  • 批准号:
    10823723
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating epigenetic mechanisms in Down syndrome using human cellular models
使用人类细胞模型研究唐氏综合症的表观遗传机制
  • 批准号:
    10655152
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating the role of astrocyte specific NFIA during initiation and progression of AD pathogenesis
研究星形胶质细胞特异性 NFIA 在 AD 发病机制的起始和进展过程中的作用
  • 批准号:
    10722872
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
INVESTIGATING HOW NOVELTY ENHANCES FEAR LEARNING & MEMORY
调查新奇事物如何增强恐惧学习
  • 批准号:
    10580151
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating the Role of Somatic Mutations in Neurofibromatosis Brain
研究体细胞突变在神经纤维瘤病脑中的作用
  • 批准号:
    10722624
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
Investigating Symbolic Computation in the Brain: Neural Mechanisms of Compositionality
研究大脑中的符号计算:组合性的神经机制
  • 批准号:
    10644518
  • 财政年份:
    2023
  • 资助金额:
    $ 52.13万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了