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烧伤患者培养角质形成细胞炎症细胞因子及受体的基因表达谱

Gene expression profile of cytokines and receptors of inflammation from cultured keratinocytes of burned patients.

作者信息

Gragnani Alfredo, Cezillo Marcus V B, da Silva Ismael D C G, de Noronha Samuel M Ribeiro, Correa-Noronha Silvana A A, Ferreira Lydia M

机构信息

Division of Plastic Surgery, Department of Surgery, Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, SP, Brazil.

Universidade Federal de São Paulo/Escola Paulista de Medicina (UNIFESP/EPM), São Paulo, SP, Brazil.

出版信息

Burns. 2014 Aug;40(5):947-56. doi: 10.1016/j.burns.2013.11.022. Epub 2013 Dec 9.


DOI:10.1016/j.burns.2013.11.022
PMID:24331407
Abstract

INTRODUCTION: At all stages of wound healing, growth factors and cytokines play a particularly important role in the interaction with keratinocytes cellular receptors. Keratinocytes have received little attention about their potential to act as a source and target of cytokines. Changes in the cytokine levels after the burning occur prior to the metabolic abnormalities. Thus, it may be possible to develop therapeutic interventions that can mitigate the acute inflammatory response and modulating expression of these cytokines. The objective was to evaluate the expression of 84 genes mediators of the inflammatory response by using PCR array in a primary human epidermal cultured keratinocytes from patients with burns. METHODS: Keratinocytes cultured from normal skin around injury from small and large burn patient were treated for DNA synthesis. The samples were analyzed by the PCR Superarray(®) assay and curve analyses were performed for 84 relevant human genes and their involvement in the inflammatory cytokines pathway and receptors. These genes were checked for the up or down regulation. And it was used MetaCore™ for the analysis of networks and Gene Ontology (GO) processes. RESULTS: Chemokines of the CXC family were more expressed in the large burn group, except CXCL12. The C, CC and CX3C chemokine family were downregulated, especially in the small burn group. The interleukins IL8 and IL1B were more expressed in large burn than in small burn; except IL13RA1, IL13 and IL5RA that were downregulated, mainly in the small burn group. CONCLUSIONS: The cytokine profile showed some important differences between the large and small burn patients, and from this original database, we can create new interventional trials in acute inflammation in burns.

摘要

引言:在伤口愈合的各个阶段,生长因子和细胞因子在与角质形成细胞的细胞受体相互作用中发挥着特别重要的作用。角质形成细胞作为细胞因子的来源和靶点的潜力很少受到关注。烧伤后细胞因子水平的变化先于代谢异常出现。因此,有可能开发出能够减轻急性炎症反应并调节这些细胞因子表达的治疗干预措施。目的是通过PCR阵列评估烧伤患者原代表皮培养角质形成细胞中84种炎症反应基因介质的表达。 方法:从大小烧伤患者损伤周围正常皮肤培养的角质形成细胞用于DNA合成。通过PCR超级阵列(®)分析对样本进行分析,并对84个人类相关基因及其在炎症细胞因子途径和受体中的参与进行曲线分析。检查这些基因的上调或下调情况。并使用MetaCore™进行网络分析和基因本体(GO)过程分析。 结果:除CXCL12外,CXC家族的趋化因子在大面积烧伤组中表达更高。C、CC和CX3C趋化因子家族下调,尤其是在小面积烧伤组中。白细胞介素IL8和IL1B在大面积烧伤中比在小面积烧伤中表达更高;除IL13RA1、IL13和IL5RA主要在小面积烧伤组中下调外。 结论:细胞因子谱在大面积和小面积烧伤患者之间显示出一些重要差异,从这个原始数据库中,我们可以在烧伤急性炎症中开展新的干预试验。

相似文献

[1]
Gene expression profile of cytokines and receptors of inflammation from cultured keratinocytes of burned patients.

Burns. 2014-8

[2]
CXC and CC chemokines induced in human renal epithelial cells by inflammatory cytokines.

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[3]
Functional characterization of cultured keratinocytes after acute cutaneous burn injury.

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[4]
Keratinocyte growth factor and the expression of wound-healing-related genes in primary human keratinocytes from burn patients.

Acta Cir Bras. 2016-8

[5]
Innate and adaptive immunity gene expression of human keratinocytes cultured of severe burn injury.

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[6]
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[7]
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[8]
Th2- and to a lesser extent Th1-type cytokines upregulate the production of both CXC (IL-8 and gro-alpha) and CC (RANTES, eotaxin, eotaxin-2, MCP-3 and MCP-4) chemokines in human airway epithelial cells.

Int Arch Allergy Immunol. 2003-8

[9]
Keratinocyte growth factor, tumor necrosis factor-alpha and interleukin-1 beta gene expression in cultured fibroblasts and keratinocytes from burned patients.

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[10]
The role of interleukin-1 in wound biology. Part II: In vivo and human translational studies.

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[5]
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[8]
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[9]
Expression of pro-inflammatory genes in lesions, spleens and blood neutrophils after burn injuries in mice treated with silver sulfodiazine.

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[10]
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