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Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

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Elevated Gene Expression of Interleukin-32 Isoforms Alpha, Beta, Gamma, and Delta in the Peripheral Blood of Chronic Psoriatic Patients

Hani A Al-Shobaili et al. Diseases.

Abstract

Inflammatory-mediated reactions have been implicated as contributors in a number of dermatological disorders, including psoriasis. However, the potential of interleukin (IL)-32 and its isoforms to contribute to the pathogenesis of psoriasis remains unexplored. This study was undertaken to investigate the role of IL-32 and its isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ in the peripheral blood of psoriatic patients. The majority of chronic plaque psoriatic patients showed elevated IL-32 mRNA levels in the peripheral blood mononuclear cells (PBMCs) as compared with the levels of IL-32 mRNA in PBMCs of healthy controls (p = 0.001). To further investigate the role of elevated levels of IL-32 in psoriatic patients, IL-32 isoforms mRNAs were determined. All tested isoforms IL-32α, IL-32β, IL-32γ, and IL-32δ were overexpressed in psoriatic patients PBMCs as compared with healthy controls' PBMCs (p < 0.05). IL-32α mRNA expression was also significantly higher as compared with all other isoforms of IL-32 in PBMCs of psoriatic patients (p < 0.001). In short, this is the first study that shows the role of IL-32 and its isoforms in the peripheral blood of psoriatic patients. Our novel findings support an association between elevated levels of IL-32 and psoriasis. The data also suggest that a major proinflammatory response of IL-32 may derive from IL-32α isoform in psoriasis.

Keywords: IL-32; IL-32 isoforms; inflammation; peripheral blood; psoriasis.

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Gene expression of human interleukin (IL)-32 in the peripheral blood mononuclear cells (PBMCs) of chronic psoriatic patients. Data in column chart (A) and scattered data points chart (B,C). Expression of IL-32 mRNA was determined by real-time qRT-PCR using either GAPDH or ACTB as an endogenous control in the comparative ∆∆CT method. PS PBMCs, psoriatic patients PBMCs. NH PBMCs, normal human PBMCs; Data are representative (mean ± SD) of experiments with PBMCs obtained from psoriatic patients (n = 42) and normal healthy subjects (n = 38). # p = 0.001 versus PS PBMCs. Comparison analysis was performed using a two-tailed t-test using Mann–Whitney analysis.
Figure 2
Figure 2
Gene expression of human interleukin (IL)-32 subtypes in the peripheral blood mononuclear cells (PBMCs) of chronic psoriatic patients. (AC) Gene expression of IL-32 alpha (IL-32 α) in PS PBMCs and NH PBMCs. @ p < 0.01 versus PS PBMCs. (DF) Gene expression of IL-32 beta (IL-32 β) in PS PBMCs and NH PBMCs. $ p < 0.05 versus PS PBMCs. (GI) Gene expression of IL-32 gamma (IL-32 γ) in PS PBMCs and NH PBMCs. * p < 0.05 versus PS PBMCs. (JL) Gene expression of IL-32 delta (IL-32 δ) in PS PBMCs and NH PBMCs. # p < 0.05 versus PS PBMCs. Expression of IL-32 subtypes was determined by real-time qRT-PCR using either GAPDH or β-actin as an endogenous control in the comparative ∆∆CT method. Data in column chart are representative (mean ± SD) of experiments with PBMCs obtained from psoriatic patients (n = 42) and normal healthy subjects (n = 38). PS PBMCs, psoriatic patients PBMCs; NH PBMCs, normal human PBMCs. Comparison analysis was performed using a two-tailed t-test using Mann–Whitney analysis.
Figure 3
Figure 3
Overexpression of IL-32α mRNA in the peripheral blood mononuclear cells (PBMCs) of chronic psoriasis patients. (A) Gene expression of IL-32 isoforms in PBMCs from psoriasis patients. * p < 0.001 versus IL-32α mRNA; (B) gene expression of IL-32 isoforms in PBMCs from normal human subjects. The mRNAs of IL-32 isoforms were determined by real-time qRT-PCR using either GAPDH or β-actin as an endogenous control in comparative ∆∆CT method. Results are representative (mean ± SEM) and statistical analysis was performed using one-way ANOVA followed by Tukey’s multiple comparison tests.

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