Nitric oxide paradox in asthma

Author(s)

Alexandre Castro Keller ^[1] ; Dunia Rodriguez ^[2] ; Momtchilo Russo ^[3]

Affiliation

^[1] Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Imunologia - Brasil

^[2] Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Imunologia - Brasil

^[3] Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Imunologia - Brasil

• Document type: Journal article
• Source: Memórias do Instituto Oswaldo Cruz; v. 100, p. 19-23, 2005-03-00.
• Field of knowledge: Biological Sciences - Immunology

Abstract

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 exhaled NO may be derived from constitutive NO synthase (NOS) such as endothelial (NOS 3) and neural (NOS 1) in normal airways, while increased levels of NO in asthma appear to be derived from inducible NOS2 expressed in the inflamed airways. Nevertheless, the functional role of NO and NOS isoforms in the regulation of AHR and airway inflammation in human or experimental models of asthma is still highly controversial. In the present commentary we will discuss the role of lipopolysaccharides contamination of allergens as key element in the controversy related to the regulation of NOS2 activity in experimental asthma. (AU)

• FAPESP's process: 99/03778-3 - Modulatio of polarized immune responses in immunologically or genetically manipulated animals
• Grantee: Momtchilo Russo
• Support Opportunities: Research Projects - Thematic Grants