A intervenção da célula epitelial na asma

 

Anabela Mota Pinto 1

Ana Todo-Bom 2

 

 

Resumo

Faz -se uma revisão da intervenção da célula epitelial brônquica na fisiopatologia da asma. O epitelio que reveste as vias respiratórias actua como uma barreira física, separando o meio externo do meio interno pulmonar, controla a permeabilidade intercelular e transcelular, e, deste modo, a acessibilidade dos agressores inalantes as células apresentadoras de antigenio envolvidas na resposta imunoinflamatoria. As células epiteliais unidas por tight junctions contribuem para a integridade das vias aéreas e expressam poliovirus receptor–related protein (PRR), toll like receptors (TLR) e protease -activated receptors (PAR), que reconhecem agentes bacterianos e alergenios. A sua disfuncao transforma -as em fonte de mediadores intervenientes na inflamação.

A interacção bidireccional entre, por um lado, o epitelio e os elementos constitutivos do brônquio e por outro, as partículas inaladas, tem subjacente a formação de uma unidade, com identidade propria designada EMTU – epithelial mesenchymal trophic unit.

Esta extensa intervencao coloca a célula epitelial no centro de accao da cronicidade e remodelacao do processo asmático.

As doenças infecciosas e o stress ambiental sao capazes de induzir alterações a nível da célula epitelial susceptíveis de modificar a sua resposta a estimulações futuras, nomeadamente a ampliar a resposta a outras agressões infecciosas por acção sinérgica das vias de sinalização.

O epitelio brônquico tem assim funções de barreira que lhe permite exercer uma permeabilidade selectiva, a nível intracelular e transcelular, e ainda metabolicamente activo pelas capacidade de produzir mediadores quimiotacticos e citocinas envolvidos no recrutamento e na activação celular, com repercussão na broncomotricidade e na remodelação da parede brônquica.

Palavras -chave: Asma, epitelio, inflamação.

 

 

The role of the epithelial cell in asthma

Abstract

It is done a review of the intervention of the epithelial bronchial cell in the pathophysiology of asthma. The respiratory epithelium acts as a physical barrier that separates the external environment from the pulmonary internal environment. It controls the intercellular and trans -cellular permeability and this way the accessibility of the inhaled pathogens to the antigen presenting cells involved in the immuno –inflammatory response. Epithelial cells connected by tight junctions contribute to the barrier function of the airways.

They express a poliovirus receiver – related protein (PRR), toll like receptors (TLRs) and protease-activated receptors (PARs), which recognize bacterial agents and allergens. Its dysfunction turns them into important sources of inflammatory mediators.

The bidirectional interaction between the epithelium and other bronchial wall elements with inhaled particles originates a structure with its own identity, the designated EMTU – Epithelial Mesenchymal Trophic Unit.

These observations support a central role for the epithelial cell in chronic inflammation and in the remodelling of the asthmatic process.

Infectious diseases and environmental stress can activate different cell receptors and signalling pathways that induce changes in the cell surface modifying their response to future stimulations, namely to other infectious aggressions.

The bronchial epithelium has barrier functions with selective permeability; it has metabolic activity producing cytokines and chemokines stimulating the cell’s recruitment and activation, increasing the bronchial reactivity and the remodelling of the airways.

Key-words: Asthma, epithelium, inflammation.

 

 

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1 Professora Associada com Agregação de Fisiopatologia – Faculdade de Medicina da Universidade de Coimbra

Directora do Instituto de Patologia Geral

2 Assistente Hospitalar Graduada em Imunoalergologia nos Hospitais da Universidade de Coimbra.

Doutoramento em Medicina Interna – Pneumologia pela Faculdade de Medicina da Universidade de Coimbra

 

Recebido para publicação/received for publication: 08.11.13

Aceite para publicação/accepted for publication: 08.12.30