Monica Campo Patino

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Credentials

MD, MPH

Bio

Administrator Info
Name: Ashley Fuchs
Phone: 612-624-0999
Email: fuchs@umn.edu
Fax: 612-625-2174

Summary
Monica Campo Patiño, MD, MPH., completed medical school at Universidad El Bosque in Bogotá, Colombia. She went on to complete a research fellowship at the Brigham and Women’s Hospital at Harvard Medical School in Boston, MA. She received a Master’s in Public Health at the Harvard T.H. Chan School of Public Health. Subsequently, she completed an internal medicine residency at Tufts Medical Center in Boston, MA and a fellowship in pulmonary and critical care medicine at the University of Washington in Seattle, WA.
 
Currently, Dr. Campo is an Assistant Professor in the University of Minnesota Department of Medicine in the Pulmonary, Critical Care, Allergy, and Sleep Medicine Division. Dr. Campo specializes in the treatment and management of general pulmonary and critically ill patients. She is committed to excellent and compassionate care of patients with chest problems. Dr. Campo’s research focuses on the discovery of new therapies for patients with respiratory infections. She has received independent funding from the National Institutes of Health for her research projects and has published in peer-reviewed journals as well as presented her research at international scientific meetings.
 

Research Summary

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. 

Teaching Summary

Pulmonary; tuberculosis

Clinical Summary

General pulmonary medicine