Infrastructure and Opportunity Fund Management

基础设施和机会基金IVIanimals（IOFM）核心的目的是创建 并通过新的临床研究促进NIAID申办的AADCRC之间的合作 资源开发项目;支持有希望的机会， 哮喘和过敏性疾病的病理生理学;并开发改进的疗法以减少 或阻止疾病进展。由于SA-AADCRC的重点强调了入门和 炎症途径和组织损伤的恶化，从以下角度来看： 肺炎支原体及其独特的ADP核糖基化和空泡化毒素， 社区获得性呼吸窘迫综合征毒素（CRTX），许多合作和 AADCRC成员之间存在协同增效的机会。单凭一个人的力量， 诱发哮喘样疾病和加剧过敏性炎症的地方，这一显着的致病性 因子作为潜在的唯一介质，或放大器，或在广泛的条件下的辅助因子 导致急性和慢性肺部病变。因此，M. 肺炎和其他环境触发因素可能是非常有影响力和揭示，因为M。 肺炎感染是常见的和持久的， 炎症、粘液分泌过多和高反应性。重要的是，BTX蛋白可以是 容易在哮喘患者的气道分泌物中检测到， 嗜酸性/淋巴细胞性炎症和对卵清蛋白和屋尘螨的高反应性 在小鼠模型中。与AADCRC合作，检查病毒和其他传染性疾病 污染物和过敏原可能导致理解某些人如何表现出夸大的 炎症反应是M.肺炎和肺炎支原体存在/持续存在。 此外，重组MTX和其他相关试剂可以作为有用的工具分享 在AADCRCs中研究沉淀的分子和病理生理机制， 哮喘样肺部炎症和相关病理。

The purpose of the Infrastructure and Opportunity Fund IVIanagement (lOFM) Core is to create and facilitate collaborations between NIAID-sponsored AADCRCs through new clinical researcii and resource development projects; support promising opportunities that advance an understanding of the pathophysiology of asthma and allergic diseases; and develop improved therapies to reduce or prevent disease progression. Since the focus of the SA-AADCRC emphasizes the Induction and exacerbation of Inflammatory pathways and tissue Injury, as viewed from the perspective of Mycoplasma pneumoniae and its unique ADP ribosylating and vacuolating toxin, designated Community Acquired Respiratory Distress Syndrome Toxin (CARDS TX), many collaborative and synergetic opportunities exist among AADCRC members. The ability of CARDS TX alone to both Induce asthma-like disease and exacerbate allergic Inflammation places this remarkable pathogenic factor as a potential sole mediator, or amplifier, or co-factor in a broad range of ainA/ay conditions that lead to acute and chronic pulmonary pathologies. Therefore, the relationships between M. pneumoniae and other environmental triggers could be very Impactful and revealing, as M. pneumoniae infections are common and persistent and CARDS TX produces lymphocytic Inflammation, mucous hypersecretion, and hyperreactivity. Importantly, CARDS TX protein can be readily detected in airway secretions of asthmatic subjects and by Itself exacerbates eosinophilic/lymphocytic Inflammation and hyperresponsiveness to ovalbumin and house dust mite In the murine model. Collaborations with AADCRCs that examine viral and other Infectious pollutants and allergens could lead to understanding how certain individuals manifest exaggerated Inflammatory responsiveness as a result of M. pneumoniae and CARDS TX presence/persistence. Also, recombinant CARDS TX and other related reagents could serve as useful tools to share among AADCRCs for studying the molecular and pathophysiological mechanisms that precipitate asthma-like pulmonary Inflammation and associated pathologies.