IL-4 up-regulates epidermal chemotactic, angiogenic, and pro-inflammatory genes and down-regulates antimicrobial genes in vivo and in vitro: Relevant in the pathogenesis of atopic dermatitis

Bao, Lei; Shi, Vivian Y.; Chan, Lawrence S.

doi:10.1016/j.cyto.2012.10.031

Cited by 58 publications

(46 citation statements)

References 50 publications

(58 reference statements)

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“…However, although IL‐25 is associated with eosinophilic inflammation, lesional CTCL skin – in all cases with heavy eosinophilic infiltration – did not show high expression of IL‐25 (Table S2; see Supporting Information). IL‐25 expression in skin was upregulated in IL‐4 transgenic mice and IL‐4 increased IL‐25 mRNA expression by HaCaT human keratinocyte cells . We examined the effect of Th2 cytokines – IL‐4 and IL‐13 – on IL‐25 production by NHEK.…”

Section: Resultsmentioning

confidence: 99%

“…As skin barrier dysfunction is shown in CTCL, as well as AD, such allergens can cause upregulation of IL‐25 expression by epidermal keratinocytes. Other than environmental factors, IL‐25 mRNA expression was upregulated in HaCaT cells, one of the cell lines of epidermal keratinocytes, after IL‐4 stimulation, suggesting that Th2 cytokines can regulate IL‐25 expression on epidermal keratinocytes. Similarly, we found that IL‐4 and IL‐13 increased IL‐25 mRNA expression by NHEK, whereas IFN‐γ, IL‐17 and TNF‐α did not.…”

Section: Discussionmentioning

confidence: 99%

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Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

et al. 2018

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

et al. 2018

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“…Briefly, NHK were stimulated for 24 h with 10 µg/mL polyinosinic/polycytidylic acid (poly I:C) and 3 ng/mL of each cytokine, tumor necrosis factor alpha (TNFα), IL-4, and IL-13 (R&D Systems, Lille, France). In order to characterize the pattern of mRNA expression in the present model of stimulated NHK, the expression of 23 mRNA, including 21 mRNA encoding various factors known to be differentially regulated in AD, such as for inflammation and keratinocyte differentiation mediators, and two housekeeping genes ( RPL13A and GAPDH ) were studied 27. The relative quantity of mRNA expression after stimulation with poly I:C and cytokines was calculated compared with that obtained from unstimulated NHK using the formula 2 −∆∆Ct were ∆Ct = Ct gene of interest − Ct housekeeping gene and ∆∆Ct=∆Ct treated − DCt control .…”

Section: Methodsmentioning

confidence: 99%

Anti-inflammatory and immunomodulatory effects of <em>Aquaphilus dolomiae</em> extract on in vitro models

Ariès

Hernandez-Pigeon

Vaissiere

et al. 2016

CCID

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BackgroundAtopic dermatitis (AD) is a common skin disease characterized by recurrent pruritic inflammatory skin lesions resulting from structural and immune defects of the skin barrier. Previous studies have shown the clinical efficacy of Avène thermal spring water in AD, and a new microorganism, Aquaphilus dolomiae was suspected to contribute to these unique properties. The present study evaluated the anti-inflammatory, antipruritic, and immunomodulatory properties of ES0, an original biological extract of A. dolomiae, in immune and inflammatory cell models in order to assess its potential use in the treatment of AD.Materials and methodsAn ES0 extract containing periplasmic and membrane proteins, peptides, lipopolysaccharides, and exopolysaccharides was obtained from A. dolomiae. The effects of the extract on pruritus and inflammatory mediators and immune mechanisms were evaluated by using various AD cell models and assays.ResultsIn a keratinocyte model, ES0 inhibited the expression of the inflammatory mediators, thymic stromal lymphopoietin, interleukin (IL)-18, IL-4R, IL-8, monocyte chemoattractant protein-3, macrophage inflammatory protein-3α, and macrophage-derived chemokine and induced the expression of involucrin, which is involved in skin barrier keratinocyte terminal differentiation. In addition, ES0 inhibited protease-activated receptor-2 activation in HaCaT human keratinocytes stimulated by stratum corneum tryptic enzyme and T helper type (Th) 1, Th2, and Th17 cytokine production in Staphylococcal enterotoxin B–stimulated CD4+ lymphocytes. Lastly, ES0 markedly activated innate immunity through toll-like receptor (TLR) 2, TLR4, and TLR5 activation (in recombinant human embryonic kidney 293 cells) and through antimicrobial peptide induction (psoriasin, human beta-defensin-2, and cathelicidin), mainly through TLR5 activation (in normal human keratinocytes).ConclusionOverall, these in vitro results confirm the marked regulatory activity of this A. dolomiae extract on inflammatory and immune responses, which may be of value by virtue of its potential as an adjunctive treatment of AD inflammatory and pruritic lesions.

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“…At the same time, neovascularization was rarely avoided in HCC, and many research gradually uncovered a link between CCL24 and VEGFA must be existed. One study reported CCL24 and VEGFA synchronously increased in 370 genes analysis of atopic dermatitis disease, one kind of chronic inflammatory skin disease [29]; whereas patients with myalgic encephalomyelitis/chronic fatigue syndrome appeared opposite outcome, VEGFA was reduced along with increases of CCL24 concentrations in plasma levels [30]; and In AMD disease, Takeda found the cause of choroidal neovascular endothelial cells drove from the trafficking of CCL24 to its downstream CCR3 [18]. …”

Section: Discussionmentioning

confidence: 99%

CCL24 contributes to HCC malignancy via RhoB- VEGFA-VEGFR2 angiogenesis pathway and indicates poor prognosis

et al. 2016

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CCL24 is one chemotactic factor extensively studied in airway inflammation and colorectal cancer but less studied in hepatocellular carcinoma (HCC) retrospectively. So HCC tissue microarray (TMA) was used to estimate relationship between CCL24 and prognosis, cell experiments were conducted to study its influence for HCC cell biological behavior. CCL24 was injected to nude mice to monitor tumor formation and pulmonary metastasis; qRT-PCR, western blot and Immunohistochemistry were used to explore potential mechanism. CCL24 plays roles in target cells via its downstream CCR3, or it is regulated by Type 2 helper T cells (Th2 cell) factors, so immune related experiments were conducted. Meanwhile, Rho GTPase family have close relation not only with T cell priming, but with neovascularization; CCL24 contributes to neovascularization in age-related macular degeneration via CCR3, so Rho GTPase family, Th2 cell factors, Human Umbilical Vein Endothelial Cells were used to uncover their trafficking. Ultimate validation was confirmed by small interfering RNA. Results showed CCL24 expression was higher in caner tissues than adjacent normal tissues, it could contribute to proliferation, migration, and invasion in HCCs, could accelerate pulmonary metastasis, promote HUVECs tube formation. Th2 cell factors were irrelevant with CCL24 in HCCs; and RhoB, VEGFA, and VEGFR2 correlated with CCL24 in both mRNA and protein level. Downstream RhoB-VEGFA signaling pathway was validated by siRhoB and siVEGFA inhibition. In a word, CCL24 contributes to HCC malignancy via RhoB-VEGFA-VEGFR2 angiogenesis pathway and indicates poor prognosis, which urges us to study further CCL24 effects on diagnosis and potential therapy for HCC.

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IL-4 up-regulates epidermal chemotactic, angiogenic, and pro-inflammatory genes and down-regulates antimicrobial genes in vivo and in vitro: Relevant in the pathogenesis of atopic dermatitis

Cited by 58 publications

References 50 publications

Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

Interleukin-25 is involved in cutaneous T-cell lymphoma progression by establishing a T helper 2-dominant microenvironment

Anti-inflammatory and immunomodulatory effects of <em>Aquaphilus dolomiae</em> extract on in vitro models

CCL24 contributes to HCC malignancy via RhoB- VEGFA-VEGFR2 angiogenesis pathway and indicates poor prognosis

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