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Vol. 46. Issue S4.
EPOC: de la etiopatogenia al tratamiento
Pages 9-15 (September 2010)
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Vol. 46. Issue S4.
EPOC: de la etiopatogenia al tratamiento
Pages 9-15 (September 2010)
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EPOC: inflamación bronquial y sistémica
COPD: bronchial and systemic inflammation
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10603
Ciro Casanova Macarioa,
Corresponding author
ccasanova@canarias.org

Autor para correspondencia.
, Juan Pablo de Torres Tajesb, Elizabeth Córdoba Lanusc
a Servicio de Neumología, Unidad de Investigación, Hospital Universitario La Candelaria, Santa Cruz de Tenerife, España
b Servicio de Neumología, Clínica Universitaria de Navarra, Pamplona, España
c Unidad de Investigación, Hospital Universitario La Candelaria, Santa Cruz de Tenerife, España
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La enfermedad pulmonar obstructiva crónica (EPOC) se considera una enfermedad inflamatoria de la vía aérea, en la que puede coexistir una inflamación sistémica de bajo grado. La etiología es multifactorial, pero, fundamentalmente, condicionada por una respuesta inflamatoria amplificada y anómala al humo del tabaco. En esta respuesta están involucradas la inmunidad innata y la adquirida. Esta última es de característica linfocitaria tipo Th1 (CD8) y su presencia parece asociarse a la progresión a estadios avanzado de la enfermedad. En la actualidad, desconocemos si la inflamación bronquial y sistémica están relacionadas o si actúan como compartimentos independientes. La mayor parte de los datos que tenemos sobre la EPOC se obtienen de estudios transversales, por lo que no se puede establecer una relación de causalidad entre los posibles mediadores inflamatorios y los factores genéticos involucrados en la afectación pulmonar y extrapulmonar de esta enfermedad. Necesitamos nuevos estudios que nos permitan categorizar la respuesta inflamatoria con los diferentes fenotipos de la EPOC.

Palabras clave:
Enfermedad pulmonar obstructiva crónica
Inflamación
Inmunidad
Genética
Abstract

Chronic obstructive pulmonary disease (COPD) is considered to be an inflammatory disease of the airways, in which there can be low-grade systemic inflammation. The etiology of this disease is multifactorial but is mainly due to an anomalous and amplified inflammatory response to tobacco smoke. This inflammatory response involves innate and acquired immunity. The latter is characterized by a Th1-type (CD8) response and its presence seems to be associated with progression to advanced stages of the disease. Currently, it is unknown whether bronchial and systemic inflammation are related or whether they act as independent compartments. Most of the available data on COPD are drawn from cross-sectional studies and consequently a causal relation between the possible inflammatory mediators and the genetic factors involved in pulmonary and extrapulmonary involvement in this disease cannot be established. Further studies are required that would allow the inflammatory response to be correlated with the distinct COPD phenotypes.

Keywords:
Chronic obstructive pulmonary disease
Inflammation
Immunity
Genetics
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