{"id":5132,"date":"2025-03-07T21:25:41","date_gmt":"2025-03-07T20:25:41","guid":{"rendered":"https:\/\/secuah.web.uah.es\/2025\/?p=348"},"modified":"2025-03-07T21:25:41","modified_gmt":"2025-03-07T20:25:41","slug":"dianas-2025-14-1-e202503x013-fernandez-vega-etal-inflammation-and-neurodegeneration-in-multiple-sclerosis-the-role-of-neutrophils-nets-and-the-nlrp3-inflammasome","status":"publish","type":"post","link":"https:\/\/dianas.web.uah.es\/journal\/dianas-2025-14-1-e202503x013-fernandez-vega-etal-inflammation-and-neurodegeneration-in-multiple-sclerosis-the-role-of-neutrophils-nets-and-the-nlrp3-inflammasome\/","title":{"rendered":"dianas 14 (1) Fern\u00e1ndez-Vega etal 2025 Inflammation and Neurodegeneration in Multiple Sclerosis: The Role of Neutrophils, NETs, and the NLRP3 Inflammasome."},"content":{"rendered":"
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dianas 14(1)
<\/a> > Fern\u00e1ndez-Vega etal
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dianas | Vol 14 Num 1 | marzo 2025 | e202503x013
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Eva Fern\u00e1ndez-Vega, Juan Mozas-Guti\u00e9rrez, Irene Cuadrado Berrocal, Raquel Reyes Manzanas<\/p>\n\n

1. <\/b>Dpto. de Farmacolog\u00eda, Farmacognosia y Bot\u00e1nica, Facultad de Farmacia, Universidad Complutense de Madrid. Pl. de Ram\u00f3n y Cajal, s\/n, Moncloa – Aravaca, 28040 Madrid.
  2. <\/b>Dpto. de Inmunolog\u00eda, Oftalmolog\u00eda y Otorrinolaringolog\u00eda, Facultad de Medicina, Universidad Complutense de Madrid. Pl. de Ram\u00f3n y Cajal, s\/n, Moncloa – Aravaca, 28040 Madrid.
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a<\/b>
. <\/b>evfern08@ucm.es  b<\/b>
. <\/b>jmozas01@ucm.es  c<\/b>
. <\/b>icberrocal@ucm.es  d<\/b>
. <\/b>raqrey02@ucm.es<\/p>\n\n

X Congreso de Se\u00f1alizaci\u00f3n Celular, SECUAH 2025.

\nXIX Simposio de Dianas Terap\u00e9uticas.

\n17 a 21 de marzo, 2025. Universidad de Alcal\u00e1. Alcal\u00e1 de Henares, Madrid. Espa\u00f1a.
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Resumen<\/p>\n

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by progressive axonal demyelination and neurodegeneration. While the immune response in MS is primarily mediated by T lymphocytes and macrophages, growing evidence highlights the pivotal role of neutrophils in disease pathogenesis. In particular, these cells contribute to neuroinflammation through the formation of Neutrophil Extracellular Traps (NETs), which have been strongly associated with the activation of the NLRP3 inflammasome. Both mechanisms, initially recognized for their antimicrobial and inflammatory functions, have been implicated in the exacerbation of CNS damage, particularly through the destruction of the myelin sheath.
Moreover, activation of the NLRP3 inflammasome amplifies the inflammatory response by promoting neutrophil activation, enhancing NETosis, and inducing the release of key pro-inflammatory cytokines such as IL-1\u03b2 and IL-18. These processes create a self-perpetuating inflammatory loop that significantly contributes to disease progression. In this context, experimental autoimmune encephalomyelitis (EAE), the most widely used animal model for MS, has provided valuable insights into the relevance of these mechanisms. Given the growing recognition of their pathogenic role, both the NLRP3 inflammasome and NETs have emerged as promising therapeutic targets. Future research focusing on their modulation could pave the way for the development of novel treatment strategies aimed at mitigating neuroinflammation and slowing disease progression.
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