TY - JOUR
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 - http://www.scopus.com/inward/record.url?scp=84901236560&partnerID=8YFLogxK
U2 - 10.1016/j.cyto.2014.05.002
DO - 10.1016/j.cyto.2014.05.002
M3 - Article
C2 - 25022955
AN - SCOPUS:84901236560
VL - 69
SP - 1
EP - 5
JO - Cytokine
JF - Cytokine
SN - 1043-4666
IS - 1
ER -
