IL-37 and 38 signalling in gestational diabetes

Yu, Zhiyan; Liu, Jun; Zhang, Rui; Huang, Xinmei; Sun, Tiange; Wu, Yueyue; Hambly, Brett D.; Bao, Shisan

doi:10.1016/j.jri.2017.09.011

Cited by 38 publications

(28 citation statements)

References 26 publications

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“…DAB was used for visualisation of the specific target. Colonic IL-36α, IL-36β and IL-36γ production was quantified objectively using ImagePro Plus 9.1, as described [23] [24].…”

Section: Immunohistochemistrymentioning

confidence: 99%

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IL-36 s in the colorectal cancer: is interleukin 36 good or bad for the development of colorectal cancer?

Chen

Zhang

et al. 2020

BMC Cancer

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Background and aims: Colorectal cancer (CRC) is a major killer. Host immunity is important in tumorigenesis. Direct comparison among IL-36α, IL-36β and IL-36γ in the prognosis of CRC is unclear. Methods: CRC tissue arrays were generated from colorectostomy samples with TNM stage, invasion depth and the demography of these patients (n = 185). Using immunohistochemistry/histopathology, IL-36α, IL-36β and IL-36γ were determined, in comparison to non-cancer tissues. Results: A significant association was observed between colonic IL-36α, IL-36β or IL-36γ and the presence of cancer (with all P < 0.0001). Using ROC curve analysis, specificity and sensitivity of IL-36α, IL-36β or IL-36γ were confirmed, with area under the curve (AUC) values of 0.68, 0.73 and 0.65, respectively. Significant differences in survival were observed between IL-36α high and IL-36α low (P = 0.003) or IL-36γ high and IL-36γ low (P = 0.03). Survival curves varied significantly when further stratification into subgroups , on the basis of combined levels of expression of two isotypes of IL-36 was undertaken. A significant difference was observed when levels of IL-36α and IL-36β were combined (P = 0.01), or a combination of IL-36α plus IL-36γ (P = 0.002). The subgroups with a combination of IL-36α high plus IL-36β high , or IL-36α high plus IL-36γ low exhibited the longest survival time among CRC patients. In contrast, the subgroups of IL-36α low plus IL-36β high or IL-36α low plus IL-36γ high had the shortest overall survival. Using the log-rank test, IL-36α high expression significantly improved survival in patients with an invasion depth of T4 (P < 0.0001), lymph node metastasis (P = 0.04), TNM III-IV (P = 0.03) or with a right-sided colon tumour (P = 0.02). Similarly, IL-36γ low expression was significantly associated with improved survival in patients with no lymph node metastasis (P = 0.008), TNM I-II (P = 0.03) or with a left-sided colon tumour (P = 0.05). Multivariate analysis demonstrated that among IL-36α, IL-36β and IL-36γ, only IL-36α (HR, 0.37; 95% CI, 0.16-0.87; P = 0.02) was an independent factor in survival, using Cox proportional hazards regression analysis. Conclusion: IL-36α or IL-36γ are reliable biomarkers in predicting the prognosis of CRC during the later or early stages of the disease, respectively. Combining IL-36α plus IL-36γ appears to more accurately predict the postoperative prognosis of CRC patients. Our data may be useful in the management of CRC.

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“…DAB was used for visualisation of the specific target. Colonic IL-36α, IL-36β and IL-36γ production was quantified objectively using ImagePro Plus 9.1, as described [23] [24].…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…In order to obtain Integrated Option Density (IOD), these photos were measured using a macro in ImagePro Plus 9.1 software (Media Cybernetics, Rockville, MD, USA). Finally, the average of the IOD from each sample was calculated [23] [24]. The Integrated Option Density obtained was more than 10,000 in the figure.…”

Section: Photograph and Image Analysismentioning

confidence: 99%

IL-36 s in the colorectal cancer: is interleukin 36 good or bad for the development of colorectal cancer?

Chen

Zhang

et al. 2020

BMC Cancer

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“…44 Gestational diabetes mellitus (GDM) is associated with vascular dysfunction and IL-38 was found to be elevated in the umbilical arteries and veins of patients with GDM. 45 Although much more work is needed to elucidate the potential role of IL-38 in vascular disease, these studies and the observation that IL-38 can be expressed in the heart and blood vessels highlight a possible role of IL-38 in vascular disease.…”

Section: Functional Studiesmentioning

confidence: 99%

Biology of IL‐38 and its role in disease

Veerdonk

Graaf

Joosten

et al. 2017

Immunological Reviews

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IL-38 belongs to the IL-36 cytokines, which in turn are part of the IL-1 family. The first biological function of IL-38 described was blocking the activation of the IL-36R signaling similar to IL-36Ra. Since IL-36 cytokines require processing in order to become fully active, it is likely that IL-38 also must be processed to become maximally active. However, the protease(s) responsible for this is currently not known. In addition of IL-38 binding IL-36R, it has been proposed it can also interact with the co-receptor TIGIRR2. IL-38 is expressed in several tissues including tonsils, placenta, heart and brain, and IL-38 has been implicated in a wide variety of diseases including cardiovascular and autoimmune disease. Here, we discuss the discovery and biological function of IL-38, and its role in the pathogenesis of a wide variety of diseases.

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“…And Ye et al indicated that IL-37 could inhibit the production of inflammatory cytokines in systemic lupus erythematosus [ 20 ]. Moreover, in the perinatal field, Southcombe and Yu et al have demonstrated that IL-37 could be aberrantly expressed on the placenta and umbilical cord tissues in patients with preeclampsia and gestational diabetes mellitus, respectively [ 21 , 22 ]. These studies mainly focus on the differences in expression.…”

Section: Introductionmentioning

confidence: 99%

IL-37 Exerts Anti-Inflammatory Effects in Fetal Membranes of Spontaneous Preterm Birth via the NF-κB and IL-6/STAT3 Signaling Pathway

Wang

Liu

Huang

et al. 2020

Mediators of Inflammation

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Spontaneous preterm birth (sPTB), defined as delivery before 37 weeks of gestation, is thought to be a multifactorial syndrome. However, the inflammatory imbalance at the maternal-fetal interface promotes excessive secretion of inflammatory factors and induces apoptosis and degradation of the extracellular matrix (ECM), which can subsequently lead to preterm birth. As an anti-inflammatory molecule in the IL-1 family, interleukin-37 (IL-37) mainly plays an inhibiting role in a variety of inflammatory diseases. However, as a typical inflammatory disease, no previous studies have been carried out to explore the role of IL-37 in sPTB. In this study, a series of molecular biological experiments were performed in clinical samples and human amniotic epithelial cell line (Wistar Institute Susan Hayflick (WISH)) to investigate the deficiency role of IL-37 and the potential mechanism. Firstly, the results indicated that the expression of IL-37 in human peripheral plasma and fetal membranes was significantly decreased in the sPTB group. Afterward, it is proved that IL-37 could significantly suppress the production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in WISH cells. Simultaneously, once silence IL-37, LPS-induced apoptosis and activity of matrix metalloproteinases (MMPs) 2 and 9 were significantly increased. In addition, the western blot data showed that IL-37 performed its biological effects by inhibiting the NF-κB and IL-6/STAT3 pathway. In conclusion, our results suggest that IL-37 limits excessive inflammation and subsequently inhibits ECM remodeling and apoptosis through the NF-κB and IL-6/STAT3 signaling pathway in the fetal membranes.

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IL-37 and 38 signalling in gestational diabetes

Cited by 38 publications

References 26 publications

IL-36 s in the colorectal cancer: is interleukin 36 good or bad for the development of colorectal cancer?

IL-36 s in the colorectal cancer: is interleukin 36 good or bad for the development of colorectal cancer?

Biology of IL‐38 and its role in disease

IL-37 Exerts Anti-Inflammatory Effects in Fetal Membranes of Spontaneous Preterm Birth via the NF-κB and IL-6/STAT3 Signaling Pathway

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