No abstract available.
Asthma* ; Child, Preschool* ; Diagnosis* ; Humans

No abstract available.
Allergens*

No abstract available.
Chemokines* ; Dermatitis, Atopic*

No abstract available.
Asthma*

No Abstract Available.
Asthma* ; Dermatitis, Atopic*

PURPOSE: Asthma is a complex disease that is characterized by airway hyperresponsiveness (AHR), reversible airway obstruction, and inflammation, marked mainly by eosinophilic infiltration. The bulk of the evidence identifies alphaCD4(+) TH2 cells as having a pivotal role in mediating the inflammation that is central to asthma but The role of CD8(+) T cells in the development of allergic airway disease is still controversial. The purpose of this study was to investigate the role of CD8(+) T cells in the development of AHR and airway inflammation in mouse model of chronic asthma. METHODS: Mice were sensitized to OVA by i.p. injection on day 1, 14 and then challenged by OVA intranasal instillation on days 27, 28, 29 47, 61, 73, 74 and then 75 days. Anti-CD8 antibody was administered to sensitized mice by i.v. injection 2h before second sensitization, day 27 and 73. In vivo airway responsiveness was measured by whole body plethysmography (Penh) to inhaled methacholine (MCh) on day 77. Lung eosinophilia, bronchoalveolar lavage fluid (BALF) cytokine levels were also assessed. RESULTS: Sensitized and challenged mice showed significant airway eosinophilia and heightened AHR to methacholine when compared with non-sensitized animals. Administration of anti-CD8 antibody prevented both development of AHR as well as BALF eosinophilia. Treatment with anti-CD8 antibody also resulted in supression of IL-5 production in BALF. CONCLUSION: These results indicate that CD8 (+) T cell may have a potential role in the development of chronic allergic airway inflammation and development of allergen-induced airway responses in mouse model.
Airway Obstruction ; Animals ; Asthma ; Bronchoalveolar Lavage Fluid ; Eosinophilia ; Eosinophils ; Inflammation ; Interleukin-5 ; Lung ; Methacholine Chloride ; Mice ; Negotiating ; Ovum ; Plethysmography, Whole Body ; T-Lymphocytes ; Th2 Cells

No abstract available.
Animals ; Asthma* ; Mice*

Allergic rhinitis is a common disease of childhood characterized by nasal, throat, and ocular itching, rhinorrhea, sneezing, nasal congestion. Those affected with allergic rhinitis often suffer from associated inflammatory conditions of the mucosa, such as allergic conjunctivitis, rhinosinusitis, asthma, otitis media with effusion, and other atopic conditions, such as eczema and food allergies. Allergic rhinitis must be diagnosed and treated properly to prevent complications and impaired quality of life. Despite a high prevalence, allergic rhinitis isoften undiagnosed and inadequately treated, especially in the pediatric population. The first step in treatment is environmental control when appropriate. It may be difficult to eliminate all offending allergens effectively to reduce symptoms, so medications are often required. Many different classes of medications are now available, and they have been shown to be effective and safe in a large number of well-designed, clinical trials. Antihistamines are effective in treating immediate symptoms of sneezing, pruritus, watery eyes, and rhinorrhea. Second generation antihistamines are the preferred antihistamines because of their superior side effect profile. Thus, decongestants are commonly used with oral antihistamines. Intranasal corticosteroids are the most effective therapy for allergic rhinitis. Leukotriene modifier may be as effective as antihistamines in treating allergic rhinitis symptoms. Cromolyn sodium is an option for mild disease when used prophylactically, and ipratropium bromide is effective when rhinorrhea is the predominant symptom. When avoidance measures and medications are not effective, specific immunotherapy is an effective alternative. Only immunotherapy results in sustained changes in the immune system. Because of improved understanding of the pathogenesis, new and better therapies may be forthcoming. The effective treatment of allergic rhinitis in children will reduce symptoms and will improve overall health and quality of life, making a happier, healthier child.
Adrenal Cortex Hormones ; Allergens ; Asthma ; Child ; Conjunctivitis, Allergic ; Cromolyn Sodium ; Diagnosis ; Eczema ; Estrogens, Conjugated (USP) ; Food Hypersensitivity ; Histamine Antagonists ; Histamine H1 Antagonists, Non-Sedating ; Humans ; Immune System ; Immunotherapy ; Ipratropium ; Mucous Membrane ; Nasal Decongestants ; Otitis Media with Effusion ; Pharynx ; Prevalence ; Pruritus ; Quality of Life ; Rhinitis* ; Sneezing

PURPOSE: Recently many studies show early exposure during childhood growth to endotoxin (lipopolysaccharides, LPS) and/or early exposure to allergens exhibit important role in development of allergy including bronchial asthma. The aim of this study was to evaluate the role of endotoxin and allergen exposure in early life via the airways in the pathogenesis of allergic airways inflammation and airway hyperresposiveness (AHR) in mouse model of asthma. METHODS: Less than one week-old Balb/c mice was used. Groups of mice were received either a single intranasal instillation of sterile physiologic saline, 1% ovalbumin (OVA), LPS or 1.0 microgram LPS in 1% OVA. On 35th day, these animals were sensitized with 1% OVA for 10 consecutive days via the airways. Animals were challenged with ovalbumin for 3 days on 55th days, and airway inflammation, hyperresponsiveness, and cytokine expression were assessed. Measurements of airway function were obtained in unrestrained animals, using whole-body plethysmography. Airway responsiveness was expressed in terms of % enhanced pause (Penh) increase from baseline to aerosolized methacholine. Lung eosinophilia, serum OVA-IgE and bronchoalveolar lavage (BAL) fluid cytokine levels were also assessed. ANOVA was used to determine the levels of difference between all groups. Comparisons for all pairs were performed by Tukey-Kramer honest significant difference test; P values for significance were set to 0.05. RESULTS: Sensitized and challenged mice with OVA showed significant airway eosinophilia and heightened responsiveness to methacholine. Early life exposure of OVA and/or LPS via the airway prevented both development of AHR as well as bronchoalveolar lavage fluid eosinophilia. Exposure with OVA or LPS also resulted in suppression of interleukin (IL)-4, 5 production in BAL fluid and OVA specific IgE in blood. CONCLUSION: These results indicate that antigen and/or LPS exposure in the early life results in inhibition of allergic responses to OVA in this mouse model of astham. Our data show that early life exposure with OVA and/or LPS may have a protective role in the development of allergic airway inflammation and development of allergen-induced airway responses in mouse model of asthma.
Allergens ; Animals ; Asthma ; Bronchoalveolar Lavage ; Bronchoalveolar Lavage Fluid ; Eosinophilia ; Hypersensitivity ; Immunoglobulin E ; Inflammation ; Interleukins ; Lung ; Methacholine Chloride ; Mice ; Ovalbumin ; Ovum ; Plethysmography

PURPOSE: Allergic asthma is a complex syndrome of reactions within the airways characterized by bronchoconstriction, airway inflammation and airway hyperresponsiveness (AHR). There is an emerging body of knowledge defining the role of CD8 (+) T cells in the pathogenesis of allergic asthma. The role of CD8 (+) T cells in the development of allergic airway disease is still controversial. The purpose of this study was to investigate the role of CD8 (+) T cells during the induction of allergen-induced AHR and airway inflammation. METHODS: Mice were sensitized to OVA by i.p. injection on day 1, 14 and then challenged by OVA inhalation on days 24, 25, 26. Anti-CD8 antibody was administered to sensitized mice by i.v. injection 2h before second sensitization and first airway challenge. In vivo airway responsiveness was measured by whole body plethysmography (Penh) to inhaled methacholine (MCh) on day 28. Lung eosinophilia, bronchoalveolar lavage fluid (BALF) cytokine levels were also assessed. RESULTS: Sensitized and challenged mice showed significant airway eosinophilia and heightened responsiveness to methacholine when compared with nonsensitized animals. Administration of anti-CD8 antibody prevented both development of AHR as well as bronchoalveolar lavage fluid eosinophilia. Anti-CD8 antibody abolished peribronchial and perivascular infiltration of inflammatory cells. Treatment with anti-CD8 antibody also resulted in supression of IL-5 production in bronchoalveolar lavage fluid. CONCLUSION: These results indicate that CD8 (+) T cell may have a potential role in the development of allergic airway inflammation and development of allergen-induced airway responses.
Animals ; Asthma ; Bronchoalveolar Lavage Fluid ; Bronchoconstriction ; Eosinophilia ; Inflammation* ; Inhalation ; Interleukin-5 ; Lung ; Methacholine Chloride ; Mice ; Ovum ; Plethysmography, Whole Body ; T-Lymphocytes*