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Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
Published on: June 24, 2020
Nuevos conocimientos sobre la inmunología de la enfermedad pulmonar obstructiva crónica
Guy G Brusselle1, Guy F Joos, Ken R Bracke
1Laboratory for Translational Research of Obstructive Pulmonary Disease, Department of Respiratory Medicine, Ghent University Hospital and Ghent University, Ghent, Belgium. guy.brusselle@ugent.be
Lancet (London, England)
|September 13, 2011
Resumen
La enfermedad pulmonar obstructiva crónica (EPOC) implica inflamación pulmonar por irritantes inhalados. Las respuestas inmunes persisten incluso después de dejar de fumar debido a factores como la autoinmunidad y el estrés oxidativo.
Área de la Ciencia:
- Inmunología Inmunología.
- Pulmonología Pulmonología.
- Biología celular Biología celular.
Sus antecedentes:
- La enfermedad pulmonar obstructiva crónica (EPOC) se caracteriza por una inflamación pulmonar crónica.
- Las partículas y gases nocivos, principalmente el humo del cigarrillo, activan las células inmunes innatas.
- Esta activación desencadena respuestas inmunes adaptativas, lo que lleva a cambios en el tejido pulmonar.
Objetivo del estudio:
- Para explorar los mecanismos que impulsan la inflamación pulmonar persistente en la EPOC.
- Comprender el papel de varios factores en la patogénesis de la EPOC a pesar de haber dejado de fumar.
Principales métodos:
- Revisión de la literatura actual sobre la patogénesis de la EPOC.
- Análisis de las vías de activación de las células inmunes (innata y adaptativa).
- Discusión de los factores que contribuyen a la inflamación crónica.
Principales resultados:
- El humo del cigarrillo activa las células epiteliales y los macrófagos a través de los receptores de reconocimiento de patrones.
- Las células dendríticas inician la inmunidad adaptativa, incluidas las respuestas de las células T y B.
- Las infecciones amplifican y perpetúan la inflamación en la EPOC estable.
Conclusiones:
- La inflamación persistente en la EPOC es multifactorial.
- Factores como la autoinmunidad, el estrés oxidativo, la hipoxia y la desregulación del microARN contribuyen.
- Estos factores mantienen la inflamación pulmonar incluso después de dejar de fumar.
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