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

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.

Expression of CCL1 and CCL18 in atopic dermatitis and psoriasis

“…Various inflammatory cells, including both T cells and eosinophils expressing cutaneous lymphocyte‐associated antigen (CLA), CD4+ or CD8+, play an important role in initiating and progressing inflammatory reactions in AD tissue 1 . It has been shown that various cytokines and chemokines are involved in inflammatory‐cell infiltration into the lesion, and that their receptors are expressed on inflammatory cells or keratinocytes 2–5 . Colantonio et al.…”

“…1 It has been shown that various cytokines and chemokines are involved in inflammatory-cell infiltration into the lesion, and that their receptors are expressed on inflammatory cells or keratinocytes. [2][3][4][5] Colantonio et al 6 showed that expression of CCL1 and CCL18 is higher in atopic skin than in normal or pruritic skin. It has been documented that the secretion of the chemokine RANTES (regulated upon activation, normal T-cell expressed and secreted) is increased by antigens or staphylococcal enterotoxin B in peripheral monocytes in patients with AD.…”

Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma

“…First, high levels of CCL28 have been identified in the sputum and airways of humans with asthma (8,9). Second, the receptors for CCL28, CCR3, and CCR10 are expressed on eosinophils, Th2 cells, iNKT cells, and regulatory T cells, all cell types that have been associated with asthma and atopic disease (9 -14).…”

Circulating SSEA-1+ stem cell-mediated tissue repair in allergic airway inflammation

“…This result is consistent with the finding that CCL28 mRNA can be detected within normal and asthmatic lungs [ 35 ]. Although there is no evidence indicating increased CCL28 expression in asthmatic patient-derived lung tissue, a previous study reported that serum CCL28 levels in children with bronchial asthma are significantly higher than those in controls [ 9 ]. Therefore, this finding raises the possibility that CCL28 might stimulate the migration of circulating SSEA-1 + cells highly expressing CCR10 from the BM reservoir into the circulation, which then migrate into inflamed lung tissue via the CXCL11–CXCR7 axis.…”