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La estimulación del nervio vago atenúa la respuesta inflamatoria sistémica a la endotoxina
L V Borovikova1, S Ivanova, M Zhang
1The Picower Institute for Medical Research, Manhasset, New York 11030, USA. lborovikova@mindspring.com
Nature
|June 6, 2000
Resumen
El cerebro regula la inflamación a través del nervio vago. Este estudio revela una vía parasimpática donde la liberación de acetilcolina inhibe las citoquinas proinflamatorias, previniendo el choque de endotoxemia letal.
Área de la Ciencia:
- La neurociencia es la neurociencia.
- Inmunología Inmunología.
- Fisiología Fisiología Fisiología.
Sus antecedentes:
- La homeostasis se basa en el equilibrio de las respuestas pro y antiinflamatorias.
- La endotoxina de las bacterias gramnegativas desencadena la liberación letal de citoquinas.
- El sistema nervioso central regula la inflamación sistémica, pero las funciones del nervio vago eferente no están claras.
Objetivo del estudio:
- Investigar el papel de la señalización eferente del nervio vago en la modulación de las respuestas inflamatorias sistémicas.
- Para identificar una vía antiinflamatoria parasimpática no reconocida anteriormente.
Principales métodos:
- Se examinó el efecto de la acetilcolina en la liberación de citoquinas en los macrófagos humanos estimulados por lipopolisacáridos.
- Estimuló el nervio vago periférico en ratas con endotoxemia letal.
Principales resultados:
- La liberación de citoquinas proinflamatorias atenuadas por acetilcolina (TNF, IL-1beta, IL-6, IL-18) pero no por IL-10.
- La estimulación del nervio vago inhibía la síntesis de TNF y prevenía el shock en ratas endotoxémicas.
Conclusiones:
- Identificó una nueva vía parasimpática que involucra al nervio vago y la acetilcolina en el control de la inflamación.
- Esta vía ofrece un objetivo terapéutico potencial para afecciones inflamatorias como la endotoxemia.
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