Decrease in serum <scp>IL</scp>‐32 level in patients with atopic dermatitis after cyclosporine treatment

Kitayama, Naomi; Otsuka, Atsushi; Nonomura, Yumi; Nakashima, Chisa; Honda, Tetsuya; Kabashima, Kenji

doi:10.1111/jdv.14274

Cited by 8 publications

(9 citation statements)

References 10 publications

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“…In recent decades, abnormalities in the expression and production of IL-32 have been identified in many human disorders such as rheumatoid arthritis, various cancers, pulmonary tuberculosis, atopic dermatitis, leishmaniasis, etc. [ 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 ]. Importantly, an elevated IL-32 level was found in the sera of patients with atopic dermatitis, asthmatic patients, systemic lupus erythematosus, etc.…”

Section: Discussionmentioning

confidence: 99%

“…Importantly, an elevated IL-32 level was found in the sera of patients with atopic dermatitis, asthmatic patients, systemic lupus erythematosus, etc. [ 27 , 28 , 30 ], indicating that IL-32 was produced by blood cells. However, the role of IL-32 in the peripheral blood has never been investigated in psoriasis.…”

Section: Discussionmentioning

confidence: 99%

“…The proinflammatory role of IL-32 has been well reported in several disorders including rheumatoid arthritis, cancers, pulmonary tuberculosis, etc. [ 21 , 22 , 23 , 24 , 25 , 26 , 27 ], and also in many skin disorders such as atopic dermatitis, hidradenitis suppurativa, leishmaniasis, and systematic lupus erythematosus [ 28 , 29 , 30 ]. Most importantly, elevated IL-32 has also been reported in skin biopsies of psoriasis patients [ 31 ].…”

Section: Introductionmentioning

confidence: 99%

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

Al‐Shobaili

Rasheed

2018

Diseases

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

Al‐Shobaili

Rasheed

2018

Diseases

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“…We observed that IL-32 sera levels were higher in patients with PAH; on the contrary, those levels were quite undetectable in SSc patients without PAH and HCs, confirming the relevance of this cytokine in highlighting the presence of WHO group 1 PAH. It has been reported that IL-32 may play a key role in the vascular alterations occurring during iPAH and showing a proinflammatory effect in several inflammatory and autoimmune diseases [25,[33][34][35]. In fact, IL-32 has been described in the abnormal ECs, populating the plexiform lesions in the lungs from iPAH patients [25], and its production seems to promote the leukocyte recruitment via the production of pro-inflammatory cytokines, such as tumour necrosis factor-α (TNF-α), IL-1β, IL-6 and IL-8 [27], all contributing to EC injury [24,25,31].…”

Section: Discussionmentioning

confidence: 99%

“…Of interest, IL-32 has been identified in the abnormal ECs, populating the plexiform lesions in the lungs of patients with iPAH [25], and probably involved in both activation and proliferation of these ECs. Increased IL-32 levels have been found associated with [25,32,33] activity and/or severity of Behcet's disease [34], systemic lupus erythematosus and atopic dermatitis [35,36]. Presently, the role of IL-32 in SSc is still unknown; thus, we assessed the expression of IL-32 in the sera of SSc patients with PAH (WHO Group 1) and compared these values with those from SSc patients without PH and patients with iPAH.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension

et al. 2020

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Background: Pulmonary arterial hypertension (PAH) is a severe complication of systemic sclerosis (SSc), associated with a progressive elevation in pulmonary vascular resistance and subsequent right heart failure and death. Due to unspecific symptoms, the diagnosis of PAH is often delayed. On this basis, it is of great value to improve current diagnostic methods and develop new strategies for evaluating patients with suspected PAH. Interleukin-32 (IL-32) is a proinflammatory cytokine expressed in damaged vascular cells, and the present study aimed to assess if this cytokine could be a new biomarker of PAH during SSc. Methods: The IL-32 expression was evaluated in the sera and skin samples of 18 SSc-PAH patients, 21 SSc patients without PAH, 15 patients with idiopathic PAH (iPAH) and 14 healthy controls (HCs), by enzyme-linked immunosorbent assay (ELISA) and immunohistochemistry (IHC). Receiver-operating characteristic (ROC) curves were performed to evaluate the cutoff of IL-32 in identifying patients with PAH. Furthermore, in SSc patients, correlation analyses were performed between IL-32 sera levels and mean pulmonary artery pressure (mPAP) evaluated by right heart catheterization (RHC) and systolic pulmonary artery pressure (sPAP), obtained by echocardiography. Additionally, the number of skin IL-32+ cells was correlated with modified Rodnan skin score (mRSS). Results: In SSc-PAH patients, IL-32 sera levels were significantly higher when compared with SSc patients without PAH and patients affected by iPAH. The analysis of ROC curve showed that IL-32 sera levels above 11.12 pg/ml were able to predict patients with PAH (sensitivity = 90%, specificity = 100%). Furthermore, the IL-32 sera levels of patients with SSc correlated with both mPAP and sPAP. In the skin derived from SSc-PAH patients, the number of IL-32+ cells was significantly increased when compared with the skin derived from SSc patients without PAH, correlating with the mRSS. Conclusion: Our study suggested that sera determination of IL-32 may be a promising approach to evaluate the presence of PAH in SSc patients and together with longitudinal future studies could help to increase the understanding how these biomarkers mirror the vascular changes and the inflammatory process during SSc.

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IL32:A novel pro-inflammatory cytokine involved in non-segmental vitiligo pathogenesis

Farag,

Shoeib,

Koutb

et al. 2024

Human Gene

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Decrease in serum IL‐32 level in patients with atopic dermatitis after cyclosporine treatment

Cited by 8 publications

References 10 publications

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

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

Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension

IL32:A novel pro-inflammatory cytokine involved in non-segmental vitiligo pathogenesis

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