STZ causes depletion of immune cells in sciatic nerve and dorsal root ganglion in experimental diabetes

J Neuroimmunol. 2017 May 15:306:76-82. doi: 10.1016/j.jneuroim.2017.03.008. Epub 2017 Mar 11.

Abstract

Streptozotocin (STZ) treatment, a common model for inducing diabetes in rodent models, induces thermal hyperalgesia and neuronal toxicity independently of hyperglycemia by oxidizing and activating TRPA1 and TRPV1. Following treatment with STZ, CD45+ immune cells were found to be depleted in sciatic nerve (SN) and DRG in mice, prior to hyperglycemia. Macrophages were also lost in DRG and NFκB-p65-activation was increased in SN macrophages. Immune cells were significantly reduced in both SN and DRG up to three weeks, post-treatment. Loss of PNS-resident macrophages in response to STZ-mediated toxicity may affect the regenerative capacity of the nerve in response to further injury caused by diabetes.

Keywords: Diabetic neuropathy; Experimental diabetes; Macrophage; Neurotoxicity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibiotics, Antineoplastic / toxicity
  • Antigens, CD / metabolism
  • Cytokines / metabolism
  • Diabetes Mellitus, Experimental / chemically induced
  • Diabetes Mellitus, Experimental / pathology*
  • Diabetes Mellitus, Experimental / physiopathology*
  • Disease Models, Animal
  • Flow Cytometry
  • Ganglia, Spinal / drug effects
  • Ganglia, Spinal / pathology*
  • Hyperalgesia / etiology
  • Intercellular Adhesion Molecule-1 / metabolism
  • Leukocytes / pathology
  • Macrophages / drug effects
  • Macrophages / pathology
  • Mice
  • Mice, Inbred C57BL
  • Sciatic Nerve / drug effects
  • Sciatic Nerve / pathology*
  • Streptozocin / toxicity
  • Time Factors

Substances

  • Antibiotics, Antineoplastic
  • Antigens, CD
  • Cytokines
  • Intercellular Adhesion Molecule-1
  • Streptozocin