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생쥐 천식모델에서 생후 조기 알레르겐/내독소 노출이 성숙 후 알레르기 기도염증에 미치는 영향
나영호,최선희,Rha, Yeong-Ho,Choi, Sun-Hee 대한소아청소년과학회 2010 Clinical and Experimental Pediatrics (CEP) Vol.53 No.4
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 $1.0{\mu}g$ 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.
최선희 ( Sun Hee Choi ),송대진 ( Dae Jin Song ),염혜영 ( Hye Yung Yum ),박용민 ( Yong Mean Park ),나영호 ( Yeong Ho Rha1 ) 대한천식알레르기학회 2016 Allergy Asthma & Respiratory Disease Vol.4 No.4
Cough is one of the common symptoms, which is usually related to respiratory infections for children. This symptom is not considered crucial. Published data reported that the community prevalence of chronic cough in primary school children is 5%-10%, while the prevalence is likely to be higher in younger children. The cause of persistent cough should be investigated. There were significant differences in the causes and management for cough according to age. Chronic cough is defined as duration of 4 weeks or longer. Common culprits for chronic cough in children are different from those in adults. The authors reviewed articles about chronic cough of children to help improve the understanding and management for pediatric chronic cough. (Allergy Asthma Respir Dis 2016: 4:235-247)
알레르기 비염과 천식의 연관성: One Airway Disease
나영호 ( Yeong Ho Rha ),최선희 ( Sun Hee Choi ) 대한소아알레르기호흡기학회 2007 Allergy Asthma & Respiratory Disease Vol.17 No.2
Allergic rhinitis (AR) and asthma are common throughout the world, with a high burden of morbidity and cost. Research and clinical experience over the years has demonstrated that AR and asthma are linked and may therefore be manifestations of the same airway disease, rather than two distinct diseases of the nose and the lung. Similarly, some studies have demonstrated that treatment of either condition in comorbid disease may result in improvement of the other. Epidemiological study suggests that asthma and allergic rhinitis frequently occur as co-morbid conditions in the same patients, with about 80-90% of asthma patients having rhinitis symptoms and about 20-50% of patients with allergic rhinitis having asthma. Furthermore, rhinitis often precedes the onset of clinical asthma and independently increases the risk for developing asthma by up to 3-fold. Allergen provocation indicates that inflammation of the nasal and bronchial mucosa is important, because it is triggered by factors common to both mucosae and plays a pivotal role in the pathogenesis of both AR and asthma. The nasal and bronchial mucosa present similarities, and most patients with asthma also have rhinitis, suggesting the concept of one airway disease. Although several mechanisms have been proposed to explain the path-ophysiological link between the upper and the lower airways, the precise mechanisms underlying the link between AR and asthma are not clearly understood. The patterns of inflammation, when stable or in response to experimental allergen challenge, are similar in the upper and lower airways. Moreover, both asthma and AR may be associated with evidence of systemic inflammation. The progresses achieved in the cellular and molecular biology of airways diseases has documented that inflammation has a important role in the pathogenesis of asthma and rhinitis. The same inflammatory cells seem to be present in the nasal and bronchial mucosa. These findings highlight the potential for improving asthma outcomes by following a combined therapeutic approach to comorbid allergic rhinitis and asthma rather than targeting each condition separately. [Pediatr Allergy Respir Dis(Korea) 2007;17:85-96]