Infrastructure and Opportunity Fund Management

基础设施和机会基金IVIanagement(LOFM)核心的目的是创建 并通过新的临床研究促进NIAID赞助的AADCRC之间的合作 和资源开发项目；支持有希望的机会，促进了解 哮喘和过敏性疾病的病理生理学；并开发改进的治疗方法，以减少 或者阻止疾病的发展。由于SA-AADCRC的重点强调归纳和 从炎症途径和组织损伤的角度来看 肺炎支原体及其独特的ADP核糖化和空泡化毒素，指定 社区获得性呼吸窘迫综合征毒素(CARD TX)，许多合作和 AADCRC成员之间存在协同合作的机会。卡TX单独对两者的能力 诱发哮喘样疾病和加重过敏性炎症 在多种AINA/AY条件下，作为潜在的唯一中介或放大因素或辅助因素的因素 会导致急性和慢性肺部病变。因此，M。 肺炎和其他环境诱因可能非常有影响力和启发性，就像M。 肺炎是常见且持续的感染，卡介苗TX可产生淋巴细胞 炎症、粘液高分泌和高反应性。重要的是，CARDS TX蛋白可以 在哮喘患者的呼吸道分泌物中很容易检测到，并本身加剧 嗜酸性/淋巴细胞性炎症和对卵白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会导致理解某些人是如何表现出夸张的 肺炎支原体和卡介苗存在/持续引起的炎症反应。 此外，重组卡TX和其他相关试剂也可以作为有用的工具来分享 在研究沉淀的分子和病理生理机制的AADCRCs中 哮喘样肺部炎症及相关病理。

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.