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

doi:10.1016/j.cyto.2014.05.002

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^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

21 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 language	English
Pages (from-to)	1-5
Number of pages	5
Journal	Cytokine
Volume	69
Issue number	1
DOIs	https://doi.org/10.1016/j.cyto.2014.05.002
Publication status	Published - 2014 Sept

Bibliographical note

Funding Information:
This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST: 2012R1A2A1A01001791) and S Kim received support from the Konkuk University research support program.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Glucose tolerance test
IL-32γ transgenic mice
Inflammatory cytokine
Pancreas
Streptozotocin (STZ)-induced type I diabetes

ASJC Scopus subject areas

Molecular Biology
Hematology
Biochemistry
Immunology and Allergy
Immunology

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10.1016/j.cyto.2014.05.002

Cite this

@article{17d7bb2a23534da69d1b63b24fedd14a,

title = "IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes",

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.",

keywords = "Glucose tolerance test, IL-32γ transgenic mice, Inflammatory cytokine, Pancreas, Streptozotocin (STZ)-induced type I diabetes",

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

note = "Funding Information: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST: 2012R1A2A1A01001791) and S Kim received support from the Konkuk University research support program.",

year = "2014",

month = sep,

doi = "10.1016/j.cyto.2014.05.002",

language = "English",

volume = "69",

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journal = "Cytokine",

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T1 - IL-32γ overexpression accelerates streptozotocin (STZ)-induced type 1 diabetes

AU - Jhun, Hyunjhung

AU - Choi, Jida

AU - Hong, Jaewoo

AU - Lee, Siyoung

AU - Kwak, Areum

AU - Kim, Eunsom

AU - Jo, Seunghyun

AU - Ryoo, Soyoon

AU - Lim, Yoojung

AU - Yoon, Do Young

AU - Hong, Jin Tae

AU - Kim, Tae Sung

AU - Lee, Youngmin

AU - Song, Keeho

AU - Kim, Soohyun

N1 - Funding Information: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MEST: 2012R1A2A1A01001791) and S Kim received support from the Konkuk University research support program.

PY - 2014/9

Y1 - 2014/9

N2 - 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.

AB - 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.

KW - Glucose tolerance test

KW - IL-32γ transgenic mice

KW - Inflammatory cytokine

KW - Pancreas

KW - Streptozotocin (STZ)-induced type I diabetes

UR - https://www.scopus.com/pages/publications/84901236560

U2 - 10.1016/j.cyto.2014.05.002

DO - 10.1016/j.cyto.2014.05.002

M3 - Article

C2 - 25022955

AN - SCOPUS:84901236560

SN - 1043-4666

VL - 69

SP - 1

EP - 5

JO - Cytokine

JF - Cytokine

IS - 1

ER -

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

Abstract

Bibliographical note

UN SDGs

Keywords

ASJC Scopus subject areas

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