NADPH Oxidase 2 Regulates NLRP3 Inflammasome Activation in the Brain after Traumatic Brain Injury

Figure 12

NOX2 deletion significantly attenuates TBI-induced TXNIP expression and complex formation within the injured mouse cortex. (a) Expression of TXNIP in the injured cortex after TBI. Representative images from sham, WT, and NOX2 KO mice show that TBI increases expression of TXNIP in the injured cortex after TBI, and TXNIP colocalizes with NLRP3 expression. Deletion of NOX2 attenuates the expression of TXNIP in the injured cortex at the 4-day post-TBI. Immunoreactivity from all images has been quantified to the right of the representative panel (data presented as fold change relative to shams). n = 4, 6, and 6 mice (sham, WT, and KO, resp.). (b) In situ PLA demonstrating NLRP3-TXNIP complex formation after TBI and regulation by NOX2. Representative confocal images of Duolink in situ co-IP show red fluorescence indicative of NLRP3-TXNIP protein-protein interaction in the injured cortex at the 4-day post-TBI. Mice deficient in NOX2 show reduced NLRP3-TXNIP complex formation at the 4-day post-TBI in the injured cortex. Quantification of all Duolink images shows significantly increased NLRP3-TXNIP interaction after TBI that is attenuated by NOX2 deletion. n = 4, 6, and 6 mice (sham, WT, and KO, resp.). Scale bar represents 50 μM. Data for (a) and (b) presented as fold change relative to sham mice. (, sham versus WT TBI; ^#, ^#### WT TBI versus KO TBI).

(a)

(b)