The clarified role of interleukin-19 in the inflammatory bowel disease and          hypersensitivity: Insights from animal models and humans

Fujimoto, Yasuyuki; Aono, Kimiya; Azuma, Yasutaka

doi:10.1292/jvms.19-0149

Cited by 9 publications

(12 citation statements)

References 39 publications

(43 reference statements)

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“…Defects in IL-10 signaling have been reported to be associated with IBD, especially in children [7]. IL-19 has been found to inhibit the production of pro-inflammatory cytokines by macrophages, Th1 and Th2 cells and has been suggested to have an anti-inflammatory effect in colitis [8].…”

Section: P R E P R I N Tmentioning

confidence: 99%

“…The role of IL-19 in IBD is not fully elucidated and data from in vitro, animal, and human studies are inconsistent. Fujimoto et al described the possible anti-inflammatory effects of IL-19 in colitis [8]. Defects in IL-19 expression and an impaired response to this cytokine have been reported to possibly contribute to inflammation in active CD [36].…”

Section: P R E P R I N Tmentioning

confidence: 99%

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Pro-inflammatory and anti-inflammatory cytokines as candidate markers in the diagnosis and assessment of Crohn's disease activity

et al. 2022

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IntroductionWe evaluated the diagnostic characteristics of interleukin (IL)-12, interferon (IFN)-γ, IL-10 and IL-19, in the diagnosis and assessment of Crohn’s disease (CD) activity.Material and methodsWe studied 49 CD patients assigned to the active (33 patients) and inactive (16 patients) disease subgroups and 31 healthy controls. Serum cytokines were measured using ELISA. Cytokine levels and their multiplication results were compared between the groups and their diagnostic characteristics in were assessed.ResultsThe levels of the studied cytokines except IL-10 and their multiplication results were significantly higher in CD patients than in controls (P <0.0001-0.007) and in patients with active than inactive disease (P <0.0001-0.023). In the diagnosis of CD, the [CRP]x[IL-19] and [IL-6]x[IFN-γ] results had a specificity of 0.96, positive predictive value (PPV) 0.97 and positive likelihood ratio (LR+) 15,0 and 15.5, respectively, while serum IL-19 and the [IL-6]x[IL-12] and IFN-γ]x[IL-12] results had a sensitivity of 0.9-0.96, negative PV (NPV) 0.75-0.86 and negative LR (LR-) 0.09-0.18. The area under the ROC curve (AUC) for these markers was 0.776-0.807. In the diagnosis of active CD, the [CRP]x[IL-10] and [CRP]x[IL-19] results had a specificity of 0.98, PPV 0.96, LR+ 33.4 and 30.5, and AUC 0.896 and 0.895, respectively. Serum IFN-γ and the [CRP]x[IFN-γ], [CRP]x[IL-12] and [IFN-γ]x[IL-19] results had diagnostic sensitivity of 0.77-0.94, NPV 0.86-0.93, LR- 0.11-0.24 and AUC 0.781-0.904.ConclusionsSerum IFN-γ, IL-19 and some of the results of the studied cytokine levels multiplication showed promising diagnostic performance in the diagnosis of CD and its active form, which requires further validation.

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Section: P R E P R I N Tmentioning

confidence: 99%

Section: P R E P R I N Tmentioning

confidence: 99%

Pro-inflammatory and anti-inflammatory cytokines as candidate markers in the diagnosis and assessment of Crohn's disease activity

et al. 2022

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“…The function of IL-19 is confusing and often contradictory depending on the organization and disease [ 7 ]. IL-19 plays multiple roles in several human diseases and their animal models, such as cardiovascular disease [ 8 ], inflammatory bowel disease [ 9 ], psoriasis [ 10 ], rheumatoid arthritis [ 11 ], acute kidney injury [ 12 ], and breast cancer [ 13 ]. In respiratory diseases, IL-19, which is reported involved in inflammatory responses and causing pulmonary injury by activating lung epithelial cells [ 14 ], is positively associated with the progression of asthma [ 15 ] and chronic obstructive pulmonary disease (COPD) [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-19 Aggravates Pulmonary Fibrosis via Activating Fibroblast through TGF-β/Smad Pathway

Wang

Sun

Wang

et al. 2022

Mediators of Inflammation

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Background. Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial pneumonia disease with no cure. Communication between injured cells is triggered and maintained by a complicated network of cytokines and their receptors. IL-19 is supported by increasing evidences for a deleterious role in respiratory diseases. However, its potential role in lung fibrosis has never been explored. Methods. Bioinformatic, immunohistochemistry and western blot analysis were used to assess the expression of IL-19 in human and mouse fibrosis lung tissues. CCK-8, transwell and flow cytometry assay were utilized to analyze the effect of IL-19 on biological behaviors of lung fibroblasts. Histopathology was used to elucidate profibrotic effect of IL-19 in vivo. Results. IL-19 was upregulated in fibrosis lung tissues. IL-19 promoted lung fibroblasts proliferation and invasion, inhibited cell apoptosis, and induced differentiation of fibroblasts to the myofibroblast phenotype, which could be revised by LY2109761, a TGF-β/Smad signaling pathway inhibitor. Furthermore, we found that IL-19 aggravated lung fibrosis in murine bleomycin-induced lung fibrosis. Conclusions. Our results imply the profibrotic role for IL-19 through direct effects on lung fibroblasts and the potential of targeting IL-19 for therapeutic intervention in pulmonary fibrosis.

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“…In turn, keratinocytes express IL-19 receptors suggesting that IL-19 may act in an autocrine manner [ 32 ]. Still little is known about the molecular mechanism of IL-19 signalling in the pathogenesis of AD; IL-19 which was originally associated with the development of type 2 helper T cell-responses and it is also associated with the development of type 1 helper T cell-responses [ 33 ]. It has been proved that IL-19 increases Th2 cytokine expression in activated T cells [ 34 ].…”

Section: Introductionmentioning

confidence: 99%

Combination of FLG mutations and SNPs of IL-17A and IL-19 influence on atopic dermatitis occurrence

Klonowska¹,

Gleń²,

Nowicki³

et al. 2022

pdia

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Introduction Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease. A fresh look on the AD pathophysiology has focused on the skin barrier defect and immune dysfunctions. IL-17A and IL-19 seem to play role in AD pathogenesis. Aim The aim was to investigate associations of SNPs of IL-17A (rs2275913) and IL-19 (rs22431188) with AD features, course and occurrence. Searching for prognostic panels composed of FLG (2282del4, R501X) mutations with IL-17A and IL-19 polymorphisms. Material and methods Blood samples were collected from 239 patients with AD and 170 controls. Two SNPs, IL-17A and IL-19 and FLG null mutations were analyzed. PCR and RFLP restriction fragment length polymorphism analysis were used. SCORAD score to establish AD severity, VAS to estimate pruritus. Results None polymorphisms of studied cytokines caused more frequent AD occurrence compared to controls. We found no associations between IL-17A and IL-19 gene polymorphisms and AD severity (respectively p = 0.954; p = 0.498), IgE level ( p = 0.707; p = 0.584), VAS ( p = 0.953; p = 0.478), concomitant asthma ( p = 0.488, p = 0.764). The G/G genotype in IL-17A (rs2275913) occurrence with coexisting 2282del4 FLG gene mutation increased the AD frequency 9 times ( p = 0.0266). Conclusions The SNPs of IL-17A rs2275913 and IL-19 rs22431188 SNP seem not to have influence on AD course and occurrence while studied alone. The coexistence of GG genotype of IL-17A and 2282del4 FLG mutation may play a role as prognostic AD factor.

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The clarified role of interleukin-19 in the inflammatory bowel disease and hypersensitivity: Insights from animal models and humans

Cited by 9 publications

References 39 publications

Pro-inflammatory and anti-inflammatory cytokines as candidate markers in the diagnosis and assessment of Crohn's disease activity

Pro-inflammatory and anti-inflammatory cytokines as candidate markers in the diagnosis and assessment of Crohn's disease activity

Interleukin-19 Aggravates Pulmonary Fibrosis via Activating Fibroblast through TGF-β/Smad Pathway

Combination of FLG mutations and SNPs of IL-17A and IL-19 influence on atopic dermatitis occurrence

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