Utilize este identificador para referenciar este registo: http://hdl.handle.net/10400.4/779
Título: A intervenção da célula epitelial na asma
Outros títulos: The role of the epithelial cell in asthma
Autor: Mota-Pinto, A
Todo-Bom, A
Palavras-chave: Asma
Células Epiteliais
Data: 2009
Editora: Sociedade Portuguesa de Pneumologia
Citação: Rev Port Pneumol. 2009;15(3):461-72
Resumo: 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.
URI: http://hdl.handle.net/10400.4/779
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