No abstract available.
Glass*

No abstract available.
Bronchiolitis ; Inflammation

Although it is difficult to find a cause of chronic urticaria in children, previous studies have been identified some triggers, such as autoimmunity, physical stimuli, food and its additives, and infection. History taking and physical examination remain the best tool for identifying an underlying cause of urticaria. First investigations include a complete blood count with differential, erythrocyte sedimentation rate, and C-reactive protein in children with chronic urticaria. If physical stimuli are suspected as triggers of chronic urticaria, appropriate provocation tests can be performed. Although the frequency of autoimmune urticaria was relatively high compared to the other causes in children with chronic urticaria, it is not easy to apply routine use of autologous serum skin tests to clinical practice. Additional extensive laboratory investigations are not required in the majority of cases. Second-generation H1-antihistamines are the mainstay of treatment from current guidelines in children with chronic urticaria, and dosage can be increased if the standard dose is not effective. Data on chronic urticaria in children are scarce, and causes have been considered to be similar to those in adults. Therefore, diagnostic approaches and treatment principles of chronic urticaria in children have been derived from extrapolating data in adults. In the future, comparative studies for the causes of chronic urticaria between children and adults, and therapeutic modalities for refractory cases will be needed.
Adult ; Autoimmunity ; Blood Cell Count ; Blood Sedimentation ; C-Reactive Protein ; Child* ; Humans ; Physical Examination ; Skin Tests ; Urticaria*

No abstract available.
Asthma* ; Folic Acid* ; Gene-Environment Interaction*

No abstract available.
Child* ; Humans ; Mycoplasma pneumoniae* ; Mycoplasma* ; Pneumonia, Mycoplasma*

Postinfectious bronchiolitis obliterans (PIBO) is an irreversible obstructive lung disease characterized by subepithelial inflammation and fibrotic narrowing of the bronchioles after lower respiratory tract infection during childhood, especially early childhood. Although diagnosis of PIBO should be confirmed by histopathology, it is generally based on history and clinical findings. Irreversible airway obstruction is demonstrated by decreased forced expiratory volume in 1 second with an absent bronchodilator response, and by mosaic perfusion, air trapping, and/or bronchiectasis on computed tomography images. However, lung function tests using spirometry are not feasible in young children, and most cases of PIBO develop during early childhood. Further studies focused on obtaining serial measurements of lung function in infants and toddlers with a risk of bronchiolitis obliterans (BO) after lower respiratory tract infection are therefore needed. Although an optimal treatment for PIBO has not been established, corticosteroids have been used to target the inflammatory component. Other treatment modalities for BO after lung transplantation or hematopoietic stem cell transplantation have been studied in clinical trials, and the results can be extrapolated for the treatment of PIBO. Lung transplantation remains the final option for children with PIBO who have progressed to end-stage lung disease.
Adrenal Cortex Hormones ; Airway Obstruction ; Bronchiectasis ; Bronchioles ; Bronchiolitis Obliterans* ; Bronchiolitis* ; Child* ; Diagnosis ; Fibrosis ; Forced Expiratory Volume ; Hematopoietic Stem Cell Transplantation* ; Hematopoietic Stem Cells* ; Humans ; Infant ; Inflammation ; Lung Diseases ; Lung Diseases, Obstructive ; Lung Transplantation* ; Lung* ; Perfusion ; Respiratory Function Tests ; Respiratory Tract Infections ; Spirometry

PURPOSE: Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease with skin barrier defects and altered immune responses. Chronic inflammation leads to irreversible fibrosis in the skin and there is no treatment to completely abolish the inflammation and fibrosis. To prevent or treat the chronic process of AD, it is necessary to develop a murine model of AD that reflects the chronic process to identify the mechanism. The aims of this study were to develop a chronic AD model with a crude extract Aspergillus fumigatus (Af) antigen. METHODS: We applied Af extract (40 µg) epicutaneously to the dorsal skin of BALB/c mice for 5 consecutive days per week during a period of 5 weeks for a chronic AD model, and 5 consecutive days repeatedly with 2 weeks interval for an acute AD model. RESULTS: The clinical score and transepidermal water loss were more increased in the chronic AD model than in the acute AD model. Histologic findings showed that more increased epidermal thickness, neutrophil infiltration and hyperkeratosis in the chronic model than in the acute model. Skin fibrosis was more prominent in the chronic model than in the acute model. The mRNA expression levels of transforming growth factor (TGF)-β, thymic stromal lymphopoietin, and interleukin-33 were increased in the skin of the chronic model compared to the acute model. The levels of total IgE, Af-specific IgE, IgG1, and IgG2a were significantly increased in the chronic model compared to controls. CONCLUSION: The Af-induced chronic AD model showed prominent fibrosis and increased TGF-β expression in the skin, which suggests that these models may be useful in the research for the mechanism of the chronic process in AD.
Animals ; Aspergillus fumigatus ; Aspergillus ; Dermatitis, Atopic ; Fibrosis ; Immunoglobulin E ; Immunoglobulin G ; Inflammation ; Interleukin-33 ; Mice ; Neutrophil Infiltration ; RNA, Messenger ; Skin ; Skin Diseases ; Transforming Growth Factors ; Water

In this article, the funding resource was misprinted unintentionally.

PURPOSE: This study was undertaken to compare blood eosinophilic inflammatory markers between the acute period and clinical remission in children with upper respiratory infection (URI) -induced wheezing, and to assess the effects of atopy and age on these changes. METHODS: In 77 children with URI-induced wheezing, blood eosinophil count and serum eosinophil cationic protein (ECP) were measured during the acute wheezing phase and clinical remission period. The data were analyzed in the subgroups divided by atopy and age, respectively. RESULTS: Blood eosinophil count was significantly lower during acute period (181.6/microliter, 67.3-490.0) than that during clinical remission period (261.8/microliter, 120.7-567.7, P=0.001), and this significant eosinopenic response was found in non-atopic children (n=36) [92.2 (41.3-206.0) /microliter vs 204.5 (106.6-392.2) /microliter, P< 0.001], but not in atopic children (n=41). A significantly higher level of serum ECP was observed during acute period (15.1 microgram/L, 7.2-31.6) than during clinical remission (13.0 microgram/L, 6.6-25.7, P=0.05), and this difference was significant only in atopic children[24.2 (15.3-38.1) microgram/L vs 16.2 (8.3-31.6) microgram/L, P< 0.001]. A significant fall in blood eosinophil count during acute period was found only in children < or=4 years (n=37), while a significant rise in serum ECP was detected only in children > 4 years (n=40). However, these differences a due to dissimilar distribution of atopy in the two age groups. CONCLUSION: Our results showed different eosinophil responses to infection in non-atopic and atopic children with URI-induced wheezing. It appears that the blunted eosinopenic response in atopic children may be associated with the predominant Th2-like response to infection.
Child* ; Eosinophil Cationic Protein ; Eosinophils* ; Humans ; Respiratory Sounds*

In this study, we investigated the kinetics of tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and high mobility group box 1 (HMGB1) concentrations in a 48-h model of canine endotoxemia by lipopolysaccharide (LPS) injection. Four healthy beagles were slowly administered 1 mg/kg of LPS diluted in normal saline, while two others were administered normal saline as controls. Blood collection was performed at 0 h (baseline), 1 h and 3 h (for TNF-alpha), 6 h, 12 h, 24 h and 48 h of the experiment, and cytokine levels were determined using the sandwich ELISA method. Early increments of TNF-alpha and IL-6 were observed (< 3 h), but HMGB1 levels increased the most at 12 h of the experiment and gradually decreased until 48 h. During the whole experiment, IL-6 and HMGB1 were sustained over 12 h of LPS injection, whereas TNF-alpha decreased within 6 h of LPS injection. Taken together, canine HMGB1 levels increase relatively late (< 12 h) and sustained longer than TNF-alpha and IL-6 in response to endotoxin. This is the first study to evaluate canine HMGB1 cytokine from endotoxemia in dogs.
Animals ; Dogs ; Endotoxemia ; Enzyme-Linked Immunosorbent Assay ; HMGB1 Protein ; Interleukin-6 ; Interleukins ; Kinetics ; Tumor Necrosis Factor-alpha