Perspectivas atuais sobre inflamação e remodelamento das vias aéreas na asma e na rinite alérgica
Current perspectives on airway inflammation and remodelling in asthma and allergic rhinitis
Ruby Pawankar
Resumo
O desenvolvimento da rinite alérgica (RA) e da asma requer uma interação entre ambiente, sistema imunológico e susceptibilidade genética. Enquanto a rinite induzida por pólen é a mais característica doença alérgica mediada pela imunoglobulina E, na RA perene os desencadeantes da alergia são mais contínuos e levam à inflamação constante. Várias células e mediadores coordenam e mantêm essa inflamação. Embora a histamina ainda seja um dos principais mediadores da reação alérgica, muitos outros mediadores produzidos por diferentes tipos celulares estão envolvidos. Assim, a intrincada interação entre esses mediadores, citocinas, quimiocinas, neuropeptídeos, moléculas de adesão e várias células na forma de uma rede complexa leva ao desenvolvimento de sintomas específicos e à hiper-reatividade não específica presente na RA. A asma é caracterizada por graus variáveis de inflamação crônica e alterações estruturais nas vias aéreas que incluem denudação epitelial, metaplasia das células caliciformes, espessamento subepitelial, aumento da massa do músculo liso nas vias aéreas, aumento das glândulas brônquicas, angiogênese, e alterações nos componentes da matriz extracelular envolvendo as pequenas e grandes vias aéreas. Acredita-se que a inflamação crônica inicie e perpetue ciclos de dano e reparo tecidual na asma, embora o remodelamento também possa ocorrer em paralelo com a inflamação. Ao mesmo tempo em que RA e asma apresentam várias semelhanças em termos de perfil e resposta das células inflamatórias e dos mediadores, o remodelamento como observado na asma não é característico da RA. Na asma, as relações entre inflamação e remodelamento das vias aéreas e função pulmonar estão sendo melhor compreendidas. Uma variedade de células inflamatórias e células estruturais atuam na coordenação da inflamação e das mudanças estruturais na asma. O aumento da responsividade das vias aéreas é um marcador substituto de inflamação e pode refletir o desenvolvimento de mudanças estruturais nas vias aéreas. Tal aumento persistente da responsividade brônquica aponta para a ocorrência de remodelamento parcialmente resistente à terapia.
Palavras-chave
Abstract
The development of AR and asthma requires an interaction between the environment, immune system and genetic susceptibility. While pollen-induced rhinitis is the most characteristic IgEmediated allergic disease, in perennial allergic rhinitis the allergic triggers are more continuous, and lead to ongoing inflammation. Several cells and mediators orchestrate and maintain this inflammation. Although histamine is still one of the major mediators of the allergic reaction, many other mediators produced by different cell types are involved. Thus, the intricate interaction amongst these mediators, cytokines, chemokines, neuropeptides, adhesion molecules and various cells in the form of a complex network leads to the development of specific symptoms and the non specific hyperreactivity of allergic rhinitis. Asthma is characterized by variable degrees of chronic inflammation and structural alterations in the airways which include epithelial denudation, goblet cell metaplasia, subepithelial thickening, increased airway smooth muscle mass, bronchial gland enlargement, angiogenesis, and alterations in extracellular matrix components, involving large and small airways. Chronic inflammation is thought to initiate and perpetuate cycles of tissue injury and repair in asthma, although remodeling may also occur in parallel with inflammation. While AR and asthma share several similarities in the inflammatory cell and mediator profiles and responses, remodeling as seen in asthma is not characteristic of AR. In asthma, the relationships of airway inflammation, remodeling and lung function are becoming better understood. A variety of inflammatory cells and structural cells play a role in orchestrating the inflammation and structural changes in asthma. Increased airway responsiveness is a surrogate marker of inflammation and may reflect the development of structural changes in the airways. Such persistent increased bronchial responsiveness indicates remodeling which is partly resistant to therapy.
Keywords
References
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Submitted date:
05/26/2014
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