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PurposeThe present study investigates the long-term effects of intravenous immunoglobulin (IVIg) therapy for the treatment of moderate to severe childhood atopic dermatitis (AD). Previous research indicates that IVIg can treat severe AD; however, the effectiveness of IVIg has not been confirmed in prospective, blinded clinical trials.MethodsForty eligible children with moderate to severe AD, as defined by the criteria of Hanifin and Rajka, were enrolled in a randomized, placebo-controlled study. After the completion of an initial screening visit (V0), the patients were randomly allocated into therapy (n=30) and control (n=10) groups (V1). Thirty children were each treated with three injections of 2.0 g/kg IVIg at 1-month intervals over a 12-week period. Ten children were treated with placebo. Assessments were conducted after each injection (V2, V3, and V4) and at 3 (V5) and 6 months (V6) after completed treatment.ResultsThe disease severity index was significantly decreased at V5 compared with the value at V1 (P<0.05). There were no significant changes in the total IgE level or total eosinophil count in peripheral blood at the last injection (V4) compared with the value at V1. The interleukin (IL)-5/interferon (IFN)-γ ratio was assessed in T-helper 1 (Th1) and Th2 cells. The ratio significantly decreased between V1 and V5, after which it increased, such that the ratio at V6 was not significantly different from that at V1. Compared with the level at V1, the intercellular cell adhesion molecule-1 level at V4 did not differ significantly, but the level at V5 was lower.ConclusionsThis study suggests that IVIg therapy may clinically improve AD in patients after 3 months of therapy, but the improvement may decline by 6 months after therapy.

Background It is unclear whether the responses of refractory and common Mycoplasma pneumoniae (MP) pneumonia to macrolides differ. Hence, this study aimed to identify biomarkers that may be used to distinguish refractory and common pneumonias caused by MP in children at hospital admission. Methods The study included 123 children divided into five groups according to infection agent and treatment protocol: Group I included those with MP infection without documented viral infection, treated with only macrolides; Group II included those with MP infection without documented viral infection, treated with a combination of macrolides and methylprednisolone; Group III included those with MP infection and documented viral infection, treated with only macrolides; Group IV included those with viral pneumonia without documented MP infection; Group V was the control group composed of admitted children without MP or a documented viral infection. These five groups were further subdivided into Groups A (including Groups I, III, IV, and V) and B (Group II) according to the responses to macrolide treatment. Concentrations of cytokines interleukin 6, interleukin 17, interleukin 18, and tumor necrosis factor-α, and lactate dehydrogenase, and ferritin of all children were evaluated, and these levels were compared among the groups. Statistical comparisons were made using Kruskal Wallis test and Mann-Whitney U test. Results Serum lactate dehydrogenase, interleukin 18, and ferritin concentrations were significantly higher in Group II than in Groups I, III, IV, and V and were significantly higher in Group B than in Group A. When the serum lactate dehydrogenase concentration was 350 IU/L or higher, the sensitivity and specificity for diagnosing refractory MP pneumonia were 73 and 80%, respectively. When the interleukin 18 level was 360 pg/mL or higher, the sensitivity and specificity for diagnosing refractory MP pneumonia were 93 and 70%, respectively. When the ferritin level was 230 pg/mL or higher, the sensitivity and specificity for diagnosing refractory MP pneumonia were 67 and 67%, respectively. Conclusion These results suggest that serum lactate dehydrogenase, interleukin 18, and ferritin constitute the critical combination of biomarkers useful for predicting refractory MP pneumonia in children at hospital admission.

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Oak pollen is a major respiratory allergen in Korea, and the distribution of oak trees is expected to increase by ecological succession and climate change. One of the drivers of climate change is increasing CO, which is also known to amplify the allergy risk of weed pollen by inducing elevated allergenic protein content. However, the impact of CO concentration on tree pollen is not clearly understood due to the experimental difficulties in carrying out extended CO treatment. To study the response of pollen production of sawtooth oak trees (Quercus acutissima) to elevated levels of ambient CO, three open-top chambers at the National Institute of Forest Science in Suwon, Korea were utilized with daytime (8 am-6 pm) CO concentrations of ambient (× 1.0, ~ 400 ppm), × 1.4 (~ 560 ppm), and × 1.8 (~ 720 ppm) treatments. Each chamber had three sawtooth oak trees planted in September 2009. One or two trees per chamber matured to bloom in 2016. Five to six catkins were selected per tree and polyethylene bags were attached to collect pollen grains. The total number of catkins per tree was counted and the number and weight of pollen grains per catkin were measured. Oak allergen-Que a 1 (Allergon Co., Uppsala, Sweden)-was extracted and purified to make an ELISA kit by which the antigen levels in the pollen samples were quantified. Total pollen counts per tree of the × 1.4 and × 1.8 treatments showed significant increase of 353 and 1299%, respectively, from the × 1.0 treatment (p < 0.001). Allergenic protein contents at the × 1.4 and × 1.8 treatments also showed significant increase of 12 and 11%, respectively (p = 0.011). The × 1.8 treatment induced significant difference from the × 1.0 treatment in terms of pollen production and allergenic protein content, whereas the × 1.4 treatment showed mixed significance. In summary, the oak trees under the elevated CO levels, which are expected in the changing climate, produced significantly higher amount of pollen and allergenic protein than under the present air conditions.

The differences between respiratory syncytial virus (RSV) and influenza A virus (IFAV) in the pathogenesis of wheezing in young children have not been clearly defined. The aim of this study was to assess the contributions of RSV vs IFAV in the pathogenesis of upper airway inflammation in wheezy young children. We compared interleukin (IL)-6, IL-8, IL-11, and interferon-gamma (IFN-gamma) levels in nasopharyngeal aspirates (NPA) from non-asthmatic children with respiratory virus infections (RSV in 17 children and IFAV in 13 children), asthmatic children with viral infections (RSV in nine children, IFAV in 10 children), and 22 unaffected healthy children (controls). Levels of IL-11 in NPA from asthmatic children were significantly higher than those from non-asthmatic children with RSV infection, and RSV infection enhanced the IL-11 production in NPA significantly compared to IFAV infection. Nasopharyngeal epithelium from children with RSV infection secreted more IL-6 than that of children with IFAV infection. There was little difference in the IL-8 and IFN-gamma levels between asthmatic and non-asthmatic children with RSV or IFAV infection. In conclusion, asthma enhanced IL-11 production in RSV infection rather than IFAV infection in early childhood. There was a trend towards greater IL-6 production in RSV infection compared with IFAV infection.

Food is closely associated with the pathogenesis of atopic dermatitis. Food allergy is usually mediated by IgE antibody to specific food proteins and determination of specific IgE antibody is the basis of the common diagnostic test for food allergy. IgG4 have been reported as blocking antibody and the protective effects of blocking antibody may be clear in inhalant allergy. However, the role of IgG4 in food allergy is still a matter of debate. In this study, the clinical significance of food allergen-specific IgE/IgG4 in atopic dermatitis was investigated and compared with that of IgE. A total of 97 patients who fulfilled the diagnostic criteria for atopic dermatitis participated in this study. Skin prick test and allergy patch test were performed. Specific IgE and IgG4 concentration were measured using allergy protein chip, 'AllergyChip'. Double blinded placebo controlled food challenge test (DBPCFC) was performed for the diagnosis of allergy to milk, egg white, wheat, and soybean. DBPCFCs for milk, egg white, soybean, and wheat were performed. The positive rates were 31.7% (19/60) in milk, 36.7% (18/49) in egg white, 30.4% (7/23) in soybean, and 34.8% (8/23) in wheat. Mean IgE/IgG4 levels in DBPCFC (+) subjects is higher than those in DBPCFC (-) subjects in all food items studied. Of them, there were significantly different between two groups in egg white and wheat (Egg white in DBPCFC (+) vs. (-): 0.4 +/- 0.3 vs. 0.2 +/- 0.2, wheat in DBPCFC (+) vs. (-): 1.2 +/- 1.2 vs. 0.3 +/- 0.3, p < 0.05). Allergen-specific IgE/IgG4 may provide one of the clues to understand the mechanism of food allergy in atopic dermatitis. The present study suggests that protein microarray can be one of the useful methods to assess ongoing status of allergic diseases.