CNS inflammation and bone marrow neuropathy in type 1 diabetes

Ping Hu, Jeffrey S. Thinschmidt, Yuanqing Yan, Sugata Hazra, Ashay Bhatwadekar, Sergio Caballero, Tatiana Salazar, Jaleel A. Miyan, Wencheng Li, Andrei Derbenev, Andrea Zsombok, Maria Tikhonenko, James M. Dominguez, Susan P. McGorray, Daniel R. Saban, Michael E. Boulton, Julia V. Busik, Mohan K. Raizada, Tailoi Chan-Ling, Maria B. Grant

    Research output: Contribution to journalArticlepeer-review


    By using pseudorabies virus expressing green fluorescence protein, we found that efferent bone marrow-neural connections trace to sympathetic centers of the central nervous system in normal mice. However, this was markedly reduced in type 1 diabetes, suggesting a significant loss of bone marrow innervation. This loss of innervation was associated with a change in hematopoiesis toward generation of more monocytes and an altered diurnal release of monocytes in rodents and patients with type 1 diabetes. In the hypothalamus and granular insular cortex of mice with type 1 diabetes, bone marrow-derived microglia/macrophages were activated and found at a greater density than in controls. Infiltration of CD45+/CCR2+/GR-1 +/Iba-1+ bone marrow-derived monocytes into the hypothalamus could be mitigated by treatment with minocycline, an anti-inflammatory agent capable of crossing the blood-brain barrier. Our studies suggest that targeting central inflammation may facilitate management of microvascular complications. Copyright © 2013 American Society for Investigative Pathology.
    Original languageEnglish
    Pages (from-to)1608-1620
    Number of pages12
    JournalAmerican journal of pathology
    Issue number5
    Publication statusPublished - Nov 2013


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