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Background Mucosa-associated epithelial chemokine (MEC; CCL28) is considered to be pivotal in mediating the migration of CC chemokine receptor 3- and 10- (CCR3- and CCR10)-expressing, skin-homing, memory, cutaneous lymphocyte-associated antigen-positive (CLA+) T cells. CCL28 is selectively and continuously expressed by epidermal keratinocytes, but highly upregulated in inflammatory skin diseases, such as atopic dermatitis (AD). Aim This controlled longitudinal study was designed to evaluate the expression of CCL28 in serum in childhood AD and bronchial asthma (BA), and its possible relationship to disease severity and activity. Methods Serum CCL28 levels were measured in 36 children with AD, 23 with BA, 14 with both conditions, and 21 healthy age- and sex-matched controls. Sixteen patients in the AD group were followed up and resampled for serum CCL28 after clinical remission. Serum CCL28 levels were correlated with some AD disease activity and severity variables. Results Serum CCL28 levels in AD, whether during flare [median, 1530 pg/mL; mean ± standard deviation (SD) = 1590.4 ± 724.3 pg/mL] or quiescence (median, 1477 pg/mL; mean ± SD = 1575.2 ± 522.1 pg/mL), were significantly higher than those in healthy children (median, 301 pg/mL; 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 pg/mL; mean ± SD = 201.6 ± 109.5 pg/mL) were significantly lower than those in the AD group, and comparable with those in healthy controls. Serum CCL28 levels in severe AD were significantly higher than those in mild and moderate cases, and correlated positively with the calculated severity scores [Leicester Sign Score (LSS) and Scoring Atopic Dermatitis (SCORAD)]. CCL28 levels during the exacerbation of AD were positively correlated with the corresponding values during remission, the peripheral absolute eosinophil counts, and serum lactate dehydrogenase levels. Serum CCL28 levels were not correlated with the serum total immunoglobulin E values in AD. Conclusions Our data reinforce the concept that CCL28 might contribute to the pathogenesis of AD, probably through the selective migration and infiltration of effector/memory T-helper-2 cells in the skin. CCL28 may also represent an objective prognostic marker for disease severity. Further studies may pave the way for CCL28 antagonism among adjuvant therapeutic strategies.

Background Expression of the tumor necrosis factor (TNF) family member APRIL (a proliferation-inducing ligand) is low in normal tissues but is elevated in various autoimmune diseases. Objectives This study explored serum APRIL in children with atopic eczema (AE) during flare and quiescence. Methods A case–control study including 50 patients with AE and 40 control subjects was conducted. The severity of AE was assessed according to each of the Leicester Sign Score (LSS), the Simple Scoring System (SSS), the SCORing of Atopic Dermatitis (SCORAD) index, and the Objective SCORAD. Serum measurements of APRIL, total immunoglobulin E, and lactate dehydrogenase were obtained in all subjects. Data were obtained during both flare and quiescence in AE subjects. Data were analyzed using the Mann–Whitney U-test and Pearson's correlation coefficient. P-values of

Objectives Apoptosis is induced by binding of death receptor ligands, members of the tumor necrosis factor (TNF) superfamily, to their cognate receptors. It is suggested that TNF-related apoptosis inducing ligand (TRAIL) is involved in pathogenesis of juvenile-onset systemic lupus erythematosus (JSLE). This study aimed to assess TRAIL concentrations in sera of JSLE children and to determine their potential relationship with disease activity, anti-double-stranded DNA (anti-dsDNA) levels, neutropenia and renal involvement. Methods Circulating levels of TRAIL were measured by enzyme-linked immunosorbent assay (ELISA) in serum samples obtained from 40 JSLE patients (20 with active and 20 with inactive disease) and 20 controls. Results The mean (SEM) serum TRAIL concentration in JSLE was 1750.7 (440.2) pg/mL. Serum TRAIL concentrations in patients were higher than those in controls (P

Galectin-3 is a carbohydrate-binding protein that plays many important regulatory roles in inflammation, immunity and cancers. Recent studies indicate that galectin-3 plays a role in rheumatoid arthritis (RA) pathogenesis and progression. Therefore, we sought to characterize the expression pattern and role of galectin-3 in juvenile idiopathic arthritis (JIA) and to explore whether galectin-3 investigated in serum and synovial fluid was associated with clinical, laboratory and radiological variables of JIA disease activity and severity.Levels of galectin-3 in serum and synovial fluid from patients with JIA and controls were determined by enzyme-linked immunosorbent assay.Median (interquartile range) serum galectin-3 concentrations (ng/mL) were increasingly higher across the following groups: healthy controls (8.1 [4.9-16.7]), total JIA children with inactive disease (18.6 [9.7-28.8], P = 0.00039 vs. controls) and active disease (35.8 [15.8-60.8], P = 0.000012 vs. controls) (inactive vs. active, P = 0.00016). Highest serum expression was found in polyarthritic children. Galectin-3 concentrations in paired sera and synovial fluid samples could be related to each other. Serum and synovial concentrations of galectin-3 were positively correlated with total number of joints with active arthritis and with overall articular severity score. Patients with Larsen index and total radiographic score ≥ 1 had significant higher serum galectin-3 levels than patients with indices and scores1.These results suggest that serum levels of galectin-3 are increased in active JIA children and galectin-3 can be a new biomarker indicating JIA disease activity, severity and progression, although its increment is not disease-specific.

The costimulatory molecule OX40 and its ligand, OX40L, mediate key aspects of allergic airway inflammation in animal models of asthma, including eosinophilic airway inflammation, airway hyperresponsiveness, and T-helper type 2 (Th2) polarization. However, involvement of these molecules in Th2-dominated allergen-induced childhood asthma remains unclear. Therefore, we sought to examine OX40L expression in pediatric asthma across disease activity and attack severity. Serum OX40L concentrations were measured by ELISA in 50 children with atopic asthma (during and in between acute attacks), and in 40 healthy children serving as controls. The median and mean (SD) serum OX40L levels (1487 and 1560 [543] pg/mL) were significantly higher in asthmatic children during acute attacks in comparison with children in between attacks (731 and 689 [321] pg/mL) and in comparison with controls (193 and 157 [60.3] pg/mL). OX40L values were higher among children who presented with acute severe asthma exacerbations than in children with mild or moderate asthma exacerbations. During stability, patients with severe persistent asthma had significantly higher levels when compared with patients with moderate or mild persistent asthma. A positive correlation could be elicited between OX40L levels during exacerbations and the corresponding values during remission. Serum OX40L levels correlated negatively with peak expiratory flow rate and positively with absolute eosinophil count. Up-regulation of OX40L may play a critical role in development of childhood atopic asthma and is in favor of asthma severity. OX40L may represent a useful biomarker of monitoring allergic inflammation. OX40L is one of the most promising targets of immune intervention for treatment of these diseases.