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Fig. 11 | Journal of Neuroinflammation

Fig. 11

From: NLRP3 inflammasome-mediated choroid plexus hypersecretion contributes to hydrocephalus after intraventricular hemorrhage via phosphorylated NKCC1 channels

Fig. 11

Schematic summary of the present study. Schematic mechanism through which NLRP3/p-NKCC1-activated CSF hypersecretion contributes to hydrocephalus in the choroid plexus after hemorrhage. After hemorrhage, the NLRP3 inflammasome was activated, which could secrete IL-1β and IL-18 into the CSF. NLRP3 altered NKCC1 phosphorylation to influence transmembrane water transport. NLRP3/p-NKCC1-mediated CSF hypersecretion contributes to hydrocephalus

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Journal of Neuroinflammation

ISSN: 1742-2094