Infrastructure and Opportunity Fund Management

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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.