Comment on “Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice”

Wang, Yuanyuan; Weber, Martin; Foreman, Oded; Remy, Helga; Mracskó, Éva; Hanson, Jesse E.

doi:10.1126/scitranslmed.ade8728

Cited by 2 publications

(1 citation statement)

References 3 publications

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“…The first, a rabbit polyclonal antibody, is no longer commercially available, leaving most studies reliant on a commercially available mouse monoclonal antibody to caspase-1. However, as noted in another study (52), the similar size of murine IgG immunoglobulin components to immature and mature caspase-1 confounds detection of caspase-1 in some experimental model systems. We find that aging studies are particularly impacted by this technical limitation due to the comparatively high amount of immunoglobulin deposition observed in aged tissue (Fig S1).…”

Section: Discussionmentioning

confidence: 89%

Characterization of age-associated inflammasome activation reveals tissue specific differences in transcriptional and post-translational inflammatory responses

Talley,

Nguyen,

Van Ye

et al. 2024

Preprint

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Aging is associated with systemic chronic, low-grade inflammation, termed ‘inflammaging’. This pattern of inflammation is multifactorial and is driven by numerous inflammatory pathways, including the inflammasome. However, most studies to date have examined changes in the transcriptomes that are associated with aging and inflammaging, despite the fact that inflammasome activation is driven by a series of post-translational activation steps, culminating in the cleavage and activation of caspase-1. Here, we utilized transgenic mice expressing a caspase-1 biosensor to examine age-associated inflammasome activation in various organs and tissues to define these post-translational manifestations of inflammaging. Consistent with other studies, we observe increased inflammation, including inflammasome activation, in tissues. However, we note that the degree of inflammasome activation is not uniformly correlated with transcriptional changes commonly used as a surrogate for inflammasome activation in tissues. Furthermore, we used a skull thinning technique to monitor central nervous system inflammasome activationin vivoin aged mice and found that neuroinflammation is significantly amplified in aged mice in response to endotoxin challenge. Together, these data reveal that inflammaging is associated with both transcriptional and post-translational inflammatory pathways that are not uniform between tissues and establish new methodologies for measuring age-associated inflammasome activationin vivoandex vivo.

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Section: Discussionmentioning

confidence: 89%

Characterization of age-associated inflammasome activation reveals tissue specific differences in transcriptional and post-translational inflammatory responses

Talley,

Nguyen,

Van Ye

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Response to Comment on “Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice”

et al. 2023

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Comment on “Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice”

Abstract: We highlight potential issues with a Western blot assay using mouse anti–caspase-1 antibody to detect cleaved caspase-1 p20 subunit in mouse brain tissue lysates.

Cited by 2 publications

References 3 publications

Characterization of age-associated inflammasome activation reveals tissue specific differences in transcriptional and post-translational inflammatory responses

Characterization of age-associated inflammasome activation reveals tissue specific differences in transcriptional and post-translational inflammatory responses

Response to Comment on “Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice”

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