IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes

Hyunjhung Jhun, Jida Choi, Jaewoo Hong, Siyoung Lee, Areum Kwak, Eunsom Kim, Seunghyun Jo, Soyoon Ryoo, Yoojung Lim, Do Young Yoon, Jin Tae Hong, Tae Sung Kim, Youngmin Lee, Keeho Song, Soohyun Kim

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Interleukin-32 (IL-32) is a cytokine produced by T lymphocytes, natural killer (NK) cells, monocytes and epithelial cells. There are five splicing variants (α, β, γ, δ, and ε) and IL-32γ is the most active isoform. We generated human IL-32γ transgenic (IL-32γ TG) mice, displaying a high level of IL-32γ expression in the pancreas. We investigated the effect of IL-32γ on streptozotocin (STZ)-induced type 1 diabetes model using IL-32γ TG mice. After a suboptimal diabetogenic dose of STZ administration, IL-32γ TG mice showed significantly increased blood glucose level comparing with that of wild type (WT) mice at day 5. Inflammatory cytokines levels such as, IL-6, TNFα, IFNγ and IL-1β, in pancreas and liver lysates were accessed by a specific cytokine ELISA. The proinflammatory cytokines were significantly enhanced in the pancreas of IL-32γ TG mice comparing to that of WT mice whereas those cytokines levels in liver of IL-32γ TG and WT mice were not changed by STZ. These data indicate that the overexpression of IL-32γ contributes to initial islet β-cells injury and inflammation in pancreas and aggravates STZ-induced type 1 diabetes.

Original languageEnglish
Pages (from-to)1-5
Number of pages5
JournalCytokine
Volume69
Issue number1
DOIs
Publication statusPublished - 2014 Jan 1

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Interleukins
Streptozocin
Medical problems
Type 1 Diabetes Mellitus
Cytokines
Pancreas
Liver
Interleukin-1
Islets of Langerhans
Natural Killer Cells
Transgenic Mice
Blood Glucose
Monocytes
Interleukin-6
Protein Isoforms
T-cells
Epithelial Cells
Enzyme-Linked Immunosorbent Assay
Inflammation
T-Lymphocytes

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Hematology
  • Biochemistry
  • Molecular Biology

Cite this

Jhun, H., Choi, J., Hong, J., Lee, S., Kwak, A., Kim, E., ... Kim, S. (2014). IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes. Cytokine, 69(1), 1-5. https://doi.org/10.1016/j.cyto.2014.05.002

IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes. / Jhun, Hyunjhung; Choi, Jida; Hong, Jaewoo; Lee, Siyoung; Kwak, Areum; Kim, Eunsom; Jo, Seunghyun; Ryoo, Soyoon; Lim, Yoojung; Yoon, Do Young; Hong, Jin Tae; Kim, Tae Sung; Lee, Youngmin; Song, Keeho; Kim, Soohyun.

In: Cytokine, Vol. 69, No. 1, 01.01.2014, p. 1-5.

Research output: Contribution to journalArticle

Jhun, H, Choi, J, Hong, J, Lee, S, Kwak, A, Kim, E, Jo, S, Ryoo, S, Lim, Y, Yoon, DY, Hong, JT, Kim, TS, Lee, Y, Song, K & Kim, S 2014, 'IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes', Cytokine, vol. 69, no. 1, pp. 1-5. https://doi.org/10.1016/j.cyto.2014.05.002
Jhun, Hyunjhung ; Choi, Jida ; Hong, Jaewoo ; Lee, Siyoung ; Kwak, Areum ; Kim, Eunsom ; Jo, Seunghyun ; Ryoo, Soyoon ; Lim, Yoojung ; Yoon, Do Young ; Hong, Jin Tae ; Kim, Tae Sung ; Lee, Youngmin ; Song, Keeho ; Kim, Soohyun. / IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes. In: Cytokine. 2014 ; Vol. 69, No. 1. pp. 1-5.
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