Airway Hyperreactivity
Mostrando 1-12 de 55 artigos, teses e dissertações.
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1. Vitamin D3 levels and NLRP3 expression in murine models of obese asthma: association with asthma outcomes
Vitamin D (25(OH)D3) is an essential nutrient that plays a role in the immune system. Serum 25(OH)D3 is found to be associated with asthma. However, the role of vitamin D in obese asthma remains unclear. Therefore, we investigated the association between vitamin D levels and asthma outcomes in a murine model of obese asthma. We also evaluated NLRP3 inflammas
Braz J Med Biol Res. Publicado em: 13/11/2017
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2. EFEITO DO 1,8 CINEOL NOS PARÂMETROS DE CONTRATILIDADE DO MÚSCULO LISO TRAQUEAL E DE MECÂNICA DO SISTEMA RESPIRATÓRIO DE RATOS EXPOSTOS A FUMAÇA DO CIGARRO / EFFECT OF THE PARAMETERS 1.8 cineole muscle contractility TRACHEAL SMOOTH AND MECHANICS OF RESPIRATORY SYSTEM OF RATS EXPOSED TO CIGARETTE SMOKE OF
O 1,8-cineol é um oxido monoterpenico, antinflamatório e miorelaxante nas vias aéreas e já mostrou atividade em diversos tipos de tecidos excitáveis incluindo diversos tipos de músculo liso. Sabe-se hoje que a fumaça do cigarro é um poluente capaz de provocar doenças principalmente no trato respiratório podendo alterar o mecanismo contrátil do mú
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 23/03/2012
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3. Efeito do condicionamento físico aeróbico de moderada intensidade na inflamação pulmonar alérgica crônica e na hiperresponsividade brônquica à metacolina em cobaias sensibilizadas / Effects of aerobic physical training with moderate intensity on chronic airway inflammation and bronchial hyperresponsivity to a methacoline in sensitized guinea pig
O treinamento físico (TF) melhora a resposta imune de indivíduos saudáveis e traz benefícios para o paciente asmático, mas seu papel na resposta alérgica é desconhecido. Objetivo: Avaliar o papel do TF de moderada intensidade na inflamação pulmonar alérgica crônica. Métodos: 54 cobaias, divididas em 4 grupos: grupo controle (C) (não sensibilizad
Publicado em: 2009
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4. Toll-like receptor 4 (TLR4) na modulação da imunidade do tipo 2. / Toll-like receptor 4 (TLR4) and modulation of Th2 immunity.
Epidemiological and experimental data suggest that bacterial lipopolysaccharides (LPS) can either protect from or exacerbate allergic asthma. LPS triggers immune responses through Toll-like receptor (TLR) 4 that in turn activates two major signaling pathways via either MyD88 or TRIF adaptor proteins. LPS is a pro-Th1 adjuvant while aluminum hydroxide (Alum)
Publicado em: 2008
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5. Nitric oxide paradox in asthma
Asthma results from allergen-driven intrapulmonary Th2 response, and is characterized by intermittent airway obstruction, airway hyperreactivity (AHR), and airway inflammation. Accumulating evidence indicates that inflammatory diseases of the respiratory tract are commonly associated with elevated production of nitric oxide (NO). It has been shown that exhal
Memórias do Instituto Oswaldo Cruz. Publicado em: 2005-03
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6. Environmental tobacco smoke exposure does not prevent corticosteroids reducing inflammation, remodeling, and airway hyperreactivity in mice exposed to allergen
The ability of corticosteroids to reduce airway inflammation and improve lung function is significantly reduced in asthmatics who are tobacco smokers compared with asthmatics who are nonsmokers. As not only high levels of tobacco smoke exposure in active smokers, but also significantly lower levels of tobacco smoke exposure from passive environmental tobacco
American Physiological Society.
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7. Atropine-enhanced, antigen challenge-induced airway hyperreactivity in guinea pigs is mediated by eosinophils and nerve growth factor
Although anticholinergic therapy inhibits bronchoconstriction in asthmatic patients and antigen-challenged animals, administration of atropine 1 h before antigen challenge significantly potentiates airway hyperreactivity and eosinophil activation measured 24 h later. This potentiation in airway hyperreactivity is related to increased eosinophil activation an
American Physiological Society.
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8. Chemokines and their role in airway hyper-reactivity
Airway hyper-reactivity is a characteristic feature of many inflammatory lung diseases and is defined as an exaggerated degree of airway narrowing. Chemokines and their receptors are involved in several pathological processes that are believed to contribute to airway hyper-responsiveness, including recruitment and activation of inflammatory cells, collagen d
BioMed Central.
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9. Simvastatin Inhibits Airway Hyperreactivity: Implications for the Mevalonate Pathway and Beyond
Rationale: Statin use has been linked to improved lung health in asthma and chronic obstructive pulmonary disease. We hypothesize that statins inhibit allergic airway inflammation and reduce airway hyperreactivity via a mevalonate-dependent mechanism.
American Thoracic Society.
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10. CD4+ T helper cells engineered to produce latent TGF-β1 reverse allergen-induced airway hyperreactivity and inflammation
T helper 2 (Th2) cells play a critical role in the pathogenesis of asthma, but the precise immunological mechanisms that inhibit Th2 cell function in vivo are not well understood. Using gene therapy, we demonstrated that ovalbumin-specific (OVA-specific) Th cells engineered to express latent TGF-β abolished airway hyperreactivity and airway inflammation ind
American Society for Clinical Investigation.
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11. Viral induction of a chronic asthma phenotype and genetic segregation from the acute response
Paramyxoviral infections cause most of the acute lower respiratory tract illness in infants and young children and predispose to the development of chronic wheezing, but the relationship between these short- and long-term viral effects are uncertain. Here we show that a single paramyxoviral infection of mice (C57BL6/J strain) not only produces acute bronchio
American Society for Clinical Investigation.
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12. Retinoic acid prevents virus-induced airway hyperreactivity and M2 receptor dysfunction via anti-inflammatory and antiviral effects
Inhibitory M2 muscarinic receptors on airway parasympathetic nerves normally limit acetylcholine release. Viral infections decrease M2 receptor function, increasing vagally mediated bronchoconstriction. Since retinoic acid deficiency causes M2 receptor dysfunction, we tested whether retinoic acid would prevent virus-induced airway hyperreactivity and prevent
American Physiological Society.