Administrative Contact
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Monica Campo Patiño, MD, MPH, is a physician-scientist in the Division of Pulmonary, Critical Care, Allergy and Sleep Medicine at the University of Minnesota’s Department of Medicine. She earned her medical degree from Universidad El Bosque in Bogotá, Colombia, and holds a Master of Public Health from the Harvard T. H. Chan School of Public Health. Dr. Campo completed her internal medicine residency at Tufts Medical Center in Boston and a fellowship in pulmonary and critical care medicine at the University of Washington in Seattle.
Clinically, Dr. Campo treats general pulmonary conditions and cares for critically ill patients, with a focus on delivering compassionate, evidence-based care to individuals with respiratory diseases. Dr. Campo leads a translational research laboratory at the Center for Immunology. Her research program examines the innate immune response in the human lung, aiming to discover new therapies for respiratory infections. Her program is built on the integration of three pillars: studying cellular host–bacterial interactions, engaging with communities to enhance research relevance, and using bioinformatics to analyze complex immunologic data.
Dr. Campo’s research program focuses on the examination of regulatory innate immunity pathways of the early stages of tuberculosis, that lead to the discovery of new therapies.
Her current projects include:
A) Class I Histone Deacetylases Regulate Innate Immune Resistance to Mycobacterium tuberculosis. New therapies that target the host instead of targeting Mycobacterium tuberculosis directly, known as host-directed therapeutics, offer a promising answer to antibiotic resistance and the inability to kill non-replicating bacilli. Dr. Campo identified a selective inhibitor of histone deacetylases that controls extracellular and intracellular growth of Mycobacteria. This compound may be promising as a host directed therapeutic against tuberculosis. The goal of the current work is to search for the mechanism by which histone deacetylase inhibitors control mycobacteria replication and to study the cellular, epigenetic and genetic mechanisms of histone deacetylases regulation of Mycobacterium tuberculosis infection.
B) Mycobacterium tuberculosis-induced responses in human alveolar macrophages vs. monocyte derived macrophages: Alveolar macrophages and recruited monocyte-derived macrophages mediate early lung immune responses to Mycobacterium tuberculosis and are poised to determine the subsequent course of infection. Although previous studies documented differences between these cells, few have described cellular functions that regulate critical steps in anti-microbial responses. Dr. Campo’s team identified Mycobacterium tuberculosis-induced pathways that were specifically upregulated in human alveolar macrophages compared to macrophages. Further studies are underway to understand how these specific pathways are differentially regulated in human alveolar and peripheral macrophages.