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特应性皮炎患者血清黏膜相关上皮趋化因子:病情严重程度的特异性标志物。

Serum mucosa-associated epithelial chemokine in atopic dermatitis: a specific marker for severity.

作者信息

Ezzat M H M, Shaheen K Y

机构信息

Department of Pediatrics, Faculty of Medicine, Ain Shams University, Cairo, Egypt.

出版信息

Indian J Dermatol. 2009 Jul;54(3):229-36. doi: 10.4103/0019-5154.55630.

DOI:10.4103/0019-5154.55630
PMID:20161852
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2810687/
Abstract

BACKGROUND

Mucosa-associated epithelial chemokine (MEC; CCL28) is considered pivotal in mediating migration of CCR3 and CCR10-expressing skin-homing memory CLA(+) T cells. CCL28 is selectively and continuously expressed by epidermal keratinocytes, but highly upregulated in inflammatory skin diseases such as atopic dermatitis (AD).

AIMS

This controlled longitudinal study was designed to evaluate the expression of CCL28 serum levels in childhood AD and bronchial asthma (BA) and its possible relations to disease severity and activity.

METHODS

Serum CCL28 levels were measured in 36 children with AD, 23 children with BA, and 14 children who had both conditions as well as in 21 healthy age and gender-matched subjects serving as controls. Sixteen patients in the AD group were followed-up and re-sampled for serum CCL28 after clinical remission. Serum CCL28 levels were correlated with some AD disease activity and severity variables.

RESULTS

Serum CCL28 levels in patients with AD whether during flare (median = 1530; mean +/- SD = 1590.4 +/- 724.3 pg/ml) or quiescence (median = 1477; mean +/- SD = 1575.2 +/- 522.1 pg/ml) were significantly higher than the values in healthy children (median = 301; mean +/- SD = 189.6 +/- 92.8 pg/ml). However, the levels during flare and quiescence were statistically comparable. The serum levels in BA (median = 340; mean +/- SD = 201.6 +/- 109.5 pg/ml) were significantly lower than the AD group and comparable with the healthy control values. Serum CCL28 levels in severe AD were significantly higher as compared with mild and moderate cases and correlated positively to the calculated severity scores (LSS and SCORAD). CCL28 levels during exacerbation of AD could be positively correlated to the corresponding values during remission, the peripheral absolute eosinophil counts, and the serum lactate dehydrogenase levels. Serum CCL28 did not vary with the serum total IgE values in AD.

CONCLUSION

Our data reinforce the concept that CCL28 might share in the pathogenesis of AD probably through selective migration and infiltration of effector/memory Th2 cells into the skin. It may also represent an objective prognostic marker for disease severity. Further studies may pave the way for CCL28 antagonism among the adjuvant therapeutic strategies.

摘要

背景

黏膜相关上皮趋化因子(MEC;CCL28)被认为在介导表达CCR3和CCR10的皮肤归巢记忆CLA(+) T细胞迁移中起关键作用。CCL28由表皮角质形成细胞选择性持续表达,但在特应性皮炎(AD)等炎症性皮肤病中高度上调。

目的

本对照纵向研究旨在评估儿童AD和支气管哮喘(BA)中CCL28血清水平的表达及其与疾病严重程度和活动度的可能关系。

方法

检测了36例AD患儿、23例BA患儿、兼具两种疾病的14例患儿以及21例年龄和性别匹配的健康对照者的血清CCL28水平。对AD组的16例患者进行随访,并在临床缓解后重新采集血清CCL28样本。血清CCL28水平与一些AD疾病活动度和严重程度变量相关。

结果

AD患者在发作期(中位数 = 1530;平均±标准差 = 1590.4±724.3 pg/ml)或静止期(中位数 = 1477;平均±标准差 = 1575.2±522.1 pg/ml)的血清CCL28水平均显著高于健康儿童(中位数 = 301;平均±标准差 = 189.6±92.8 pg/ml)。然而,发作期和静止期的水平在统计学上具有可比性。BA患者的血清水平(中位数 = 340;平均±标准差 = 201.6±109.5 pg/ml)显著低于AD组,与健康对照值相当。重度AD患者的血清CCL28水平显著高于轻度和中度病例,并与计算出的严重程度评分(LSS和SCORAD)呈正相关。AD加重期的CCL28水平与缓解期的相应值、外周血嗜酸性粒细胞绝对计数以及血清乳酸脱氢酶水平呈正相关。AD患者血清CCL28水平与血清总IgE值无关。

结论

我们的数据强化了CCL28可能通过效应/记忆Th2细胞选择性迁移和浸润至皮肤而参与AD发病机制的概念。它也可能代表疾病严重程度的客观预后标志物。进一步的研究可能为辅助治疗策略中的CCL28拮抗作用铺平道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/3445efbf90fa/IJD-54-229-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/9036d62d6643/IJD-54-229-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/9312588543dc/IJD-54-229-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/7ec3d3c75380/IJD-54-229-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/ae57f8df005e/IJD-54-229-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/e03a8979ba4c/IJD-54-229-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/3445efbf90fa/IJD-54-229-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/9036d62d6643/IJD-54-229-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/9312588543dc/IJD-54-229-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/7ec3d3c75380/IJD-54-229-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/ae57f8df005e/IJD-54-229-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f508/2810687/3445efbf90fa/IJD-54-229-g006.jpg

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