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A study demonstrated that MCAO could induce NLRP1 activates caspase-1 and the amount of subsequent IL-1β
and NLRP5 inflammasome expression in rat neurons. [62] is proportional to the concentration of mutant SOD1
Traumatic brain injury patients with higher NLRP1 level added. In this process, the activation of inflammasome
in cerebrospinal fluid may have a worse prognosis. [63] requires endosomal rupture and participation of ASC.
However, it is not clear which specific inflammasome
Pyroptosis and chronic aseptic disease in the nervous system is involved. Caspase-1 or IL-1β defect would improve
Chronic aseptic diseases have a great influence on the survival rate of mice expressing toxic SOD1, which
the structure and function of CNS. MS is a typical indicates that pyroptosis and its relative mechanisms
one. In MS, T cells and macrophages move into CNS. could exacerbate ASL. [74]
A study of NLRP3 and ASC knockout mice found
that autoimmune encephalitis depends on the NLRP3 CONCLUSION
inflammasome. [64,65] Inhibition of NLRP3 expression and
subsequent reduction of IL-1β and IL-18 secretion can Recent findings of the pyroptosis and inflammasome
restrain the activation of T cell and its migration into have provided insight into a new mechanism that
CNS, so as to mitigate the autoimmune encephalitis. [64-66] may contribute to neuronal and glial cell death during
neurological diseases. Multiple potential targets
In cuprizone-induced CNS autoimmune inflammation upstream and downstream of pyroptosis signaling and
and demyelination model, IL-1β and IL-18 play a targeting its expression, assembly, activity and products,
different role in demyelination. IL-1β knockout mice may pave the way for newly therapeutic drugs that may
have a similar MS phenotype to wild-type animals, rescue inflammation in neurological diseases. However,
but the process of remyelination is delayed. This it is important to note that although some aspects of
suggests that IL-1β may promote recovery from MS. [67] the inflammatory response will not only exacerbate
In contrast, in IL-18 knockout mice, the disease is brain injury, it is also likely that other components
reduced, and the speed of myelination is faster. [68] In will provide a beneficial contribution to brain recovery.
NLRP3 knockout mice, the onset is delayed in cuprizone Elucidating the role of these components will represent
induced demyelination, but the extent of remyelination a challenge for future research. Unquestionably,
is identical to those of wild-type. [68] Therefore, the still a lot needs to be done to clarify the role of the
pyroptosis and its relative mechanisms are involved inflammasome during the recovery phase following
in the pathological process, and IL-1β and IL-18 have neurological diseases.
opposite effects on the recovery of the disease.
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