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Relationship between IL-22 and IL-22BP in diabetic cognitive dysfunction.

Xiaobai Wang1,2, Shengxue Yu1,2, Wenqiang Liu1,2

  • 1Liaoning Key Laboratory of Diabetic Cognitive and Perceptive Dysfunction, Jinzhou Medical University, Jinzhou, China.

Acta Diabetologica
|January 30, 2023
PubMed
Summary

A reduced IL-22/IL-22BP ratio contributes to diabetic cognitive dysfunction. Recombinant IL-22 (rIL-22) treatment improved learning, memory, and neuronal health in diabetic mice.

Keywords:
ApoptosisDiabetes mellitusIL-22IL-22BP

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Area of Science:

  • Neuroscience
  • Immunology
  • Endocrinology

Background:

  • CD4+ T helper 22 (Th22) cells and their cytokine IL-22 are implicated in autoimmune diseases like type 1 diabetes mellitus.
  • Interleukin-22 (IL-22) can protect neurons from apoptosis, yet cognitive decline and neuronal apoptosis occur in diabetes mellitus (DM).
  • The role of IL-22, its receptors (IL-22Rα1), and its inhibitor (IL-22BP) in diabetic encephalopathy (DE) remains unclear.

Purpose of the Study:

  • To investigate the relationship between IL-22, IL-22Rα1, and IL-22BP in the context of diabetic encephalopathy (DE).
  • To evaluate the therapeutic effects of IL-22 on hippocampal neurons, learning, and memory in a mouse model of diabetes.

Main Methods:

  • A streptozotocin-induced diabetes mouse model was used, divided into control, diabetes, diabetes + rIL-22, and diabetes + IL-22BP groups.
  • Cognitive function was assessed using the Morris water maze test.
  • Hippocampal IL-22, IL-22Rα1, IL-22BP expression, neuronal apoptosis, and protein levels were analyzed using ELISA, RT-qPCR, TUNEL, Nissl, immunofluorescence, and Western blotting.

Main Results:

  • Diabetic mice exhibited cognitive decline, hippocampal neuronal apoptosis, and altered expression of IL-22, IL-22Rα1, IL-22BP, Caspase-3, and C-caspase-3, with a decreased IL-22/IL-22BP ratio.
  • Recombinant IL-22 (rIL-22) treatment improved learning and memory, reduced neuronal apoptosis, and normalized IL-22/IL-22BP ratio and apoptosis markers in diabetic mice.
  • IL-22BP administration exacerbated cognitive deficits and hippocampal pathology in diabetic mice.

Conclusions:

  • A diminished IL-22/IL-22BP ratio is a key factor in diabetic cognitive dysfunction.
  • Recombinant IL-22 (rIL-22) demonstrates significant therapeutic potential for alleviating diabetic encephalopathy (DE).
  • Targeting the IL-22 and IL-22BP interaction offers a promising therapeutic strategy for managing DM complications.