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.

Public Health Relevance

The Infrastructure and Opportunity Fund Management Core could provide important opportunities for collaborations between the San Antonio AADCRC and other Centers, as Mycoplasma pneumoniae and its ADP ribosylating and vacuolating toxin (CARDS TX) induce and exacerbate allergic inflammation. Therefore, lOFM Core-supported collaborations that link the SA-AADCRC with other Centers studying inflammatory triggers of asthma and allergic diseases could lead to innovative therapies and improved diagnostic assessments of patient wellness and prognosis.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
5U19AI070412-07
Application #
8378303
Study Section
Special Emphasis Panel (ZAI1-PA-I)
Project Start
Project End
Budget Start
2012-08-01
Budget End
2013-07-31
Support Year
7
Fiscal Year
2012
Total Cost
$738,034
Indirect Cost
$272,284
Name
University of Texas Health Science Center San Antonio
Department
Type
DUNS #
800772162
City
San Antonio
State
TX
Country
United States
Zip Code
78229
Ramasamy, Kumaraguruparan; Balasubramanian, Sowmya; Manickam, Krishnan et al. (2018) Mycoplasma pneumoniae Community-Acquired Respiratory Distress Syndrome Toxin Uses a Novel KELED Sequence for Retrograde Transport and Subsequent Cytotoxicity. MBio 9:
Maselli, Diego J; Medina, Jorge L; Brooks, Edward G et al. (2018) The Immunopathologic Effects of Mycoplasma pneumoniae and Community-acquired Respiratory Distress Syndrome Toxin. A Primate Model. Am J Respir Cell Mol Biol 58:253-260
Segovia, Jesus A; Chang, Te-Hung; Winter, Vicki T et al. (2018) NLRP3 Is a Critical Regulator of Inflammation and Innate Immune Cell Response during Mycoplasma pneumoniae Infection. Infect Immun 86:
Benedetto, Roberta; Ousingsawat, Jiraporn; Wanitchakool, Podchanart et al. (2017) Epithelial Chloride Transport by CFTR Requires TMEM16A. Sci Rep 7:12397
Steed, Ashley L; Christophi, George P; Kaiko, Gerard E et al. (2017) The microbial metabolite desaminotyrosine protects from influenza through type I interferon. Science 357:498-502
Sundaram, Aparna; Chen, Chun; Khalifeh-Soltani, Amin et al. (2017) Targeting integrin ?5?1 ameliorates severe airway hyperresponsiveness in experimental asthma. J Clin Invest 127:365-374
Wood, Pamela R; Kampschmidt, Jordan C; Dube, Peter H et al. (2017) Mycoplasma pneumoniae and health outcomes in children with asthma. Ann Allergy Asthma Immunol 119:146-152.e2
Shen, Haiqian; Gonzalez-Juarbe, Norberto; Blanchette, Krystle et al. (2016) CD8(+) T cells specific to a single Yersinia pseudotuberculosis epitope restrict bacterial replication in the liver but fail to provide sterilizing immunity. Infect Genet Evol 43:289-96
Buchheit, Kathleen M; Cahill, Katherine N; Katz, Howard R et al. (2016) Thymic stromal lymphopoietin controls prostaglandin D2 generation in patients with aspirin-exacerbated respiratory disease. J Allergy Clin Immunol 137:1566-1576.e5
Cahill, Katherine N; Raby, Benjamin A; Zhou, Xiaobo et al. (2016) Impaired E Prostanoid2 Expression and Resistance to Prostaglandin E2 in Nasal Polyp Fibroblasts from Subjects with Aspirin-Exacerbated Respiratory Disease. Am J Respir Cell Mol Biol 54:34-40

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