RePORT India Partners:

  • Mater Research Institute-University of Queensland, Translational Research Institute, Woolloongabba, Queensland, Australia
  • Department of Science and Technology/National Research Foundation Centre of Excellence for Biomedical TB Research/Medical Research Council Centre for Molecular and Cellular Biology, Division of Molecular Biology and Human Genetics, Faculty of Medicine and Health Sciences, Stellenbosch University, Tygerberg, South Africa.
  • Department of Internal Medicine and Radboud Center for Infectious Diseases, Radbourd University Medical Center, Nijmegen, the Netherlands.
  • Population Health Research Institute, St George's, University of London, UK.
  • Division of Diabetes, Endocrinology, and Metabolic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
  • Department of Microbial Infection and Immunity, Ohio State University, Columbus, OH.
  • World Diabetes Foundation, Copenhagen, Denmark.
  • Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO.
  • Department of Medicine, University of Massachusetts Medical School, Worcester, MA.
  • School of Public Health, University of Texas Health Science Center Houston, Brownsville, TX.


Ronacher, K., et al. (2017). "Defining a Research Agenda to Address the Converging Epidemics of Tuberculosis and Diabetes: Part 2: Underlying Biologic Mechanisms." Chest 152(1): 174-180.


There is growing interest in the re-emerging interaction between type 2 diabetes (DM) and TB, but the underlying biologic mechanisms are poorly understood despite their possible implications in clinical management. Experts in epidemiologic, public health, basic science, and clinical studies recently convened and identified research priorities for elucidating the underlying mechanisms for the co-occurrence of TB and DM. We identified gaps in current knowledge of altered immunity in patients with DM during TB, where most studies suggest an underperforming innate immunity, but exaggerated adaptive immunity to Mycobacterium tuberculosis. Various molecular mechanisms and pathways may underlie these observations in the DM host. These include signaling induced by excess advanced glycation end products and their receptor, higher levels of reactive oxidative species and oxidative stress, epigenetic changes due to chronic hyperglycemia, altered nuclear receptors, and/or differences in cell metabolism (immunometabolism). Studies in humans at different stages of DM (no DM, pre-DM, and DM) or TB (latent or active TB) should be complemented with findings in animal models, which provide the unique opportunity to study early events in the host-pathogen interaction. Such studies could also help identify biomarkers that will complement clinical studies in order to tailor the prevention of TB-DM, or to avoid the adverse TB treatment outcomes that are more likely in these patients. Such studies will also inform new approaches to host-directed therapies.

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Ronacher K, van Crevel R, Critchley JA, Bremer AA, Schlesinger LS, Kapur A, Basaraba R, Kornfeld H, Restrepo BI
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