Analysis of eotaxin 1/CCL11, eotaxin 2/CCL24 and eotaxin 3/CCL26 expression in lesional and non-lesional skin of patients with atopic dermatitis

Owczarek, Witold; Paplińska, Magdalena; Targowski, Tomasz; Jahnz-Różyk, Karina; Paluchowska, Elwira; Kucharczyk, Aleksandra; Kasztalewicz, Beata

doi:10.1016/j.cyto.2010.02.016

Cited by 37 publications

(25 citation statements)

References 43 publications

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“…Among the 100 most dramatically upregulated genes, we found that the mRNA level of the T H 2 chemokine CCL26, which might be involved in the pathogenesis of AD, 35,36 was significantly upregulated by the addition of IL-4/IL-13 (see Table E1 in this article's Online Repository at www.jacionline.org, rank 2). It has been reported that the production of CCL26 is induced by T H 2 cytokines in cells of the keratinocyte cell line HaCaT.…”

Section: Resultsmentioning

confidence: 95%

The Janus kinase inhibitor JTE-052 improves skin barrier function through suppressing signal transducer and activator of transcription 3 signaling

Amano

Nakajima

Kunugi

et al. 2015

Journal of Allergy and Clinical Immunology

200

187

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Section: Resultsmentioning

confidence: 95%

The Janus kinase inhibitor JTE-052 improves skin barrier function through suppressing signal transducer and activator of transcription 3 signaling

Amano

Nakajima

Kunugi

et al. 2015

Journal of Allergy and Clinical Immunology

200

187

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“…IL-4 binding to either receptor mediates the phosphorylation and dimerization of the Signal Transducer and Activator of Transcription 6 (STAT6), regulating transcriptional activation of genes in target cells 9 . Keratinocytes exposed to IL-4 exhibit reduced expression of Epidermal Differentiation Complex (EDC) genes 13 , decreased expression of defensins 3 , altered expression of keratins 14 , and increased production of the chemokine CCL26 (eotaxin 3) 15 .…”

Section: Introductionmentioning

confidence: 99%

IL-4 impairs wound healing potential in the skin by repressing fibronectin expression

Serezani

Bozdoğan

Sehra

et al. 2017

Journal of Allergy and Clinical Immunology

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Background Atopic dermatitis (AD) is characterized by intense pruritis and is a common childhood inflammatory disease. Many factors are known to affect AD development, including the pleiotropic cytokine interleukin (IL)-4. Yet, still little is known regarding the direct effects of IL-4 on keratinocyte function. Objective and Methods: In this report, RNA-seq and functional assays were used to define the impact of the allergic environment on primary keratinocyte function and wound repair in mice. Results Acute or chronic stimulation by IL-4 modified expression of over 1000 genes expressed in human keratinocytes that are involved in a broad spectrum of non-overlapping functions. Among the IL-4-induced changes, repression of fibronectin critically impaired the human keratinocyte wounding response. Moreover, in mouse models of spontaneous and induced AD-like lesions there was delayed re-epithelialization. Importantly, topical treatment with fibronectin restored the epidermal repair response. Conclusion Keratinocyte gene expression is critically shaped by IL-4, altering cell fate decisions likely important for the clinical manifestations and pathology of allergic skin disease.

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“…CCR3 is mainly presented on eosinophils, and is also found on basophils, monocytes, Th2 lymphocytes, epithelial cells as well as airway smooth muscles (Zhebrun et al 2014). Thus, CCL24 is considered a contributor to kinds of atopic disorders, parasitic infections and numerous systemic diseases (Owczarek et al 2010, Kinoshita et al 2012.…”

Section: Introductionmentioning

confidence: 99%

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Meng

Shang

et al. 2015

Reproduction

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Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation. Reproduction (2015) 150 417-427

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Analysis of eotaxin 1/CCL11, eotaxin 2/CCL24 and eotaxin 3/CCL26 expression in lesional and non-lesional skin of patients with atopic dermatitis

Cited by 37 publications

References 43 publications

The Janus kinase inhibitor JTE-052 improves skin barrier function through suppressing signal transducer and activator of transcription 3 signaling

The Janus kinase inhibitor JTE-052 improves skin barrier function through suppressing signal transducer and activator of transcription 3 signaling

IL-4 impairs wound healing potential in the skin by repressing fibronectin expression

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

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