Palabras clave
Endocannabinoidoma
Cannabidiol
Neuroinmunología cutánea
Prurito
Cómo citar
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Resumen
Objetivo: Analizar los principales mecanismos fisiopatológicos de la dermatitis atópica desde una perspectiva neuroinmune, enfatizando la interacción entre disfunción de la barrera epidérmica, inflamación crónica mediada por respuestas Th2 y vías del prurito neurógeno, además del papel regulador del endocannabinoidoma y la modulación por cannabidiol. Revisión de la literatura: La dermatitis atópica resulta de la disfunción de la barrera cutánea, la hiperreactividad inmunológica y alteraciones neuroinmunes que perpetúan el prurito crónico. Citocinas como IL‑4, IL‑13 e IL‑31 comprometen la barrera epidérmica e intensifican la inflamación, mientras mediadores neurógenos amplifican la sensibilización periférica y central. El endocannabinoidoma es un sistema regulador formado por mediadores lipídicos, enzimas y receptores, incluidos TRP, PPARγ y GPR55, que modulan inflamación, diferenciación epidérmica y señalización pruritogénica. El cannabidiol regula indirectamente este sistema mediante modulación de CB1, interacción con CB2 e inhibición parcial de FAAH, favoreciendo el control de procesos inflamatorios y neuroinmunes. Consideraciones finales: El endocannabinoidoma constituye un marco relevante para comprender la relación entre inflamación, barrera epidérmica y prurito. El cannabidiol presenta potencial terapéutico prometedor, aunque aún existen lagunas científicas que exigen investigaciones más rigurosas.
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