Association between interleukin-32 gene polymorphism and susceptibility to preeclampsia

Mazlum, Fatemeh; Gharesi‐Fard, Behrouz; Hadinedoushan, Hossein; Ghashti, Yousef Bakhshizadeh

doi:10.1080/10641955.2021.1958836

Cited by 7 publications

(8 citation statements)

References 29 publications

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“…Another study conducted on a variety of alleles and genotypes showed that IL ‐ 32 SNP rs4786370 may be a risk factor for preeclampsia. 27 In addition, the C allele of rs4786370 is linked to an increase in HDL‐C levels, which can affect and possibly lower the CVD risk in rheumatoid arthritis patients. 12 However, this finding is not consistent with our finding that the T allele of rs4786370 reduces CAD risk.…”

Section: Discussionmentioning

confidence: 99%

“…Such differences are likely due to differences in ethnicity, sample size, patient selection, clinical heterogeneity, low statistical power, or a combination of these factors. 27 Furthermore, it is required to clarify the potential relationship between plasma IL‐32 levels and the SNP in question. It has been reported that the TT genotype of rs28372698 leads to increased IL‑32γ expression in thyroid carcinoma.…”

Section: Discussionmentioning

confidence: 99%

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Effects of IL‐32 polymorphisms and IL‐32 levels on the susceptibility and severity of coronary artery disease

Jin

Liu

Wang

et al. 2021

Clinical Laboratory Analysis

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Background: Interleukin-32 (IL-32) has long been proposed as a biomarker for coronary artery disease (CAD). We aimed to evaluate the association between IL-32 levels and coronary stenosis severity, IL-32 polymorphisms rs28372698 and rs4786370, and CAD susceptibility.Methods: A total of 362 patients with definite or suspected CAD that underwent angiography were recruited (CAD group, n = 175; nonobstructive CAD group, n = 56; control group, n = 131). The severity of coronary stenosis was assessed using the Gensini score and the number of diseased vessels. IL-32 levels were determined using enzyme-linked immunosorbent assay. Gene polymorphisms were genotyped using PCR and sequencing techniques.Results: IL-32 levels were significantly different at different levels of coronary artery stenosis (p < 0.05), and logIL-32 was positively correlated with the Gensini score (r = 0.357, p < 0.01). Multivariate logistic regression analysis revealed that IL-32 was independently associated with CAD (OR = 6.526, 95% CI: 3.344-12.739, p < 0.01).The receiver operating characteristic analysis revealed the area under the curve for discriminating the CAD and Gensini score were 0.605 and 0.613, respectively. Furthermore, IL-32 levels were significantly higher before percutaneous coronary intervention (PCI) than at 7 days post-PCI (p = 0.012). The homozygous TT genotype and T allele of rs28372698 were found to be associated with increased risk of CAD, while TT homozygosity and the T allele of rs4786370 with reduced risk of CAD (p < 0.05). However, both SNPs had no obvious effect on IL-32 levels or coronary stenosis severity in patients with CAD. Conclusion:To the best of our knowledge, our study is the first to show that rs28372698 and rs4786370 are associated with CAD susceptibility in Chinese Han population. We also suggest that plasma IL-32 levels may be indicative of coronary artery stenosis and the efficacy of PCI and provide guidance for risk stratification and disease management.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of IL‐32 polymorphisms and IL‐32 levels on the susceptibility and severity of coronary artery disease

Jin

Liu

Wang

et al. 2021

Clinical Laboratory Analysis

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“…Recently, several studies have demonstrated the impact of IL-32 polymorphisms on cancer progression. Moreover, IL-32 SNPs were studied and reviewed with their association to disease outcome (90)(91)(92)(93)(94)(95), and by 2021, one review performed a meta-analysis to evaluate the SNPs in malignancy (96). Up to now, three polymorphisms of IL-32 were found to be associated with the progression of several cancers that are rs28372698, rs12934561, and rs2015620 (Table 1).…”

Section: Implications Of Il-32 Polymorphisms In Cancermentioning

confidence: 99%

A Paradoxical Effect of Interleukin-32 Isoforms on Cancer

et al. 2022

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IL-32 plays a contradictory role such as tumor proliferation or suppressor in cancer development depending on the cancer type. In most cancers, it was found that the high expression of IL-32 was associated with more proliferative and progression of cancer. However, studying the isoforms of IL-32 cytokine has placed its paradoxical role into a wide range of functions based on its dominant isoform and surrounding environment. IL-32β, for example, was found mostly in different types of cancer and associated with cancer expansion. This observation is legitimate since cancer exhibits some hypoxic environment and IL-32β was known to be induced under hypoxic conditions. However, IL-32θ interacts directly with protein kinase C-δ reducing NF-κB and STAT3 levels to inhibit epithelial-mesenchymal transition (EMT). This effect could explain the different functions of IL-32 isoforms in cancer. However, pro- or antitumor activity which is dependant on obesity, gender, and age as it relates to IL-32 has yet to be studied. Obesity-related IL-32 regulation indicated the role of IL-32 in cancer metabolism and inflammation. IL-32-specific direction in cancer therapy is difficult to conclude. In this review, we address that the paradoxical effect of IL-32 on cancer is attributed to the dominant isoform, cancer type, tumor microenvironment, and genetic background. IL-32 seems to have a contradictory role in cancer. However, investigating multiple IL-32 isoforms could explain this doubt and bring us closer to using them in therapy.

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“…In this context, a genomic functional study allows identifying the genetic variants of IL-32 ( 79 ) capable of regulating its production and influencing the development and disease outcome in tegumentary leishmaniasis. Three IL32 variants already evaluated in other diseases ( 7 , 80 – 82 ) were investigated in ATL. A Brazilian cohort of ATL patients and healthy individuals were evaluated for IL32 SNP rs4786370 (promoter region), which is associated with protection against ATL.…”

Section: Il-32 In Different Leishmaniasesmentioning

confidence: 99%

A Critical Overview of Interleukin 32 in Leishmaniases

Ribeiro‐Dias

Oliveira

2022

Front. Immunol.

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Interleukin-32 (IL-32) has several immune regulatory properties, which have driven its investigation in the context of various diseases. IL-32 expression is reported to be induced in the lesions of patients with American tegumentary leishmaniasis (ATL) by the New World Leishmania spp. that are responsible for causing ATL and visceral leishmaniasis (VL). IL-32 expression may elevate the inflammatory process through the induction of pro-inflammatory cytokines and also via mechanisms directed to kill the parasites. The genetic variants of IL-32 might be associated with the resistance or susceptibility to ATL, while different isoforms of IL-32 could be associated with distinct T helper lymphocyte profiles. IL-32 also determines the transcriptional profile in the bone marrow progenitor cells to mediate the trained immunity induced by β-glucan and BCG, thereby contributing to the resistance against Leishmania. IL-32γ is essential for the vitamin D-dependent microbicidal pathway for parasite control. In this context, the present review report briefly discusses the data retrieved from the studies conducted on IL-32 in leishmaniasis in humans and mice to highlight the current challenges to understanding the role of IL-32 in leishmaniasis.

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Association between interleukin-32 gene polymorphism and susceptibility to preeclampsia

Cited by 7 publications

References 29 publications

Effects of IL‐32 polymorphisms and IL‐32 levels on the susceptibility and severity of coronary artery disease

Effects of IL‐32 polymorphisms and IL‐32 levels on the susceptibility and severity of coronary artery disease

A Paradoxical Effect of Interleukin-32 Isoforms on Cancer

A Critical Overview of Interleukin 32 in Leishmaniases

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