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

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Author(s): Ezzat MHM | Shaheen K

Journal: Indian Journal of Dermatology
ISSN 0019-5154

Volume: 54;
Issue: 3;
Start page: 229;
Date: 2009;
Original page

Keywords: Atopy | CCL28 | mucosa-associated epithelial chemokine

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.
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