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Molecules and Pathways at the Coccidioides Host-Pathogen Interface

球孢子菌宿主-病原体界面的分子和途径

基本信息

批准号：
10364963
负责人：
Satya Dandekar
金额：
$ 173.6万
依托单位：
UNIVERSITY OF CALIFORNIA, SAN FRANCISCO
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-01-01 至 2026-12-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10364963
关键词：
Acute Antibodies Antifungal Agents Antigens Automobile Driving Behavior Biological Markers Biological Products Biology Blood California Cells Cerebrospinal Fluid Chronic Clinical Coccidioides Coccidioidomycosis Collaborations Communication Cytometry Data Data Analyses Data Set Development Diagnosis Diagnostic Disease Disease Outcome Drug Screening Foundations Fungal Antigens Future Genetic Transcription Goals Growth Human Immune Immune System Diseases Immune response Immune system Infection Learning Lung nodule Medical Meningitis Metabolic Modeling Molecular Molecular Profiling Molecular Target Mus Mycoses Nature Outcome Pathogenesis Pathway interactions Patients Pharmaceutical Preparations Research Role Sampling Source Surveys T cell response Technology Testing The science of Mycology Therapeutic Time Transcript Treatment Failure Virulence Virulence Factors cell type chronic infection desert fever eosinophil experimental study fungus immunological diversity laboratory experiment macrophage metabolomics microbial mouse model multidisciplinary mutant novel pathogen response single-cell RNA sequencing small molecule sound technological innovation therapeutic development transcriptome transcriptomics

项目摘要

Summary (Overall, Sil and Dandekar) The overarching theme of the proposed Coccidioides Collaborative Research Center (CCRC) is to identify molecules and pathways at the Coccidioides host-pathogen interface. Our long-term goal is to analyze the dialog between fungus and the host immune system in the context of models (macrophages and mice) and in the context of chronic and disseminated infections (in humans). Our expertise with basic mycology will facilitate our determination of Coccidioides factors that are critical for causing disease. Our rich source of clinical samples from the endemic region of California and our access to technological innovation will facilitate our ability to identify molecules, cells, metabolites, and pathways that correlate with a patient context that is permissive or restrictive for dissemination. Our expertise with data analysis will promote the integration of our molecular findings to generate an understanding of host response pathways that are correlated with disease state and clinical outcome. Additionally, we will evaluate the diagnostic potential of Coccidioides antigens and host biomarkers, thereby closing existing gaps in the diagnosis of coccidioidomycosis. At the same time, we will make key basic discoveries in microbial biology and host response, driving the field of fungal pathogenesis and medical mycology forward. Finally, by integrating the data from Projects and Cores, we hope to identify new molecular targets for anti-fungal development as well as host pathways that could be targeted by novel or existing biologics to tip the immune response in favor of the host.

总结（总体，Sil和Dandekar）