Autophagy and NLRP3 inflammasome crosstalk in neuroinflammation in aged bovine brains.
Davide De BiaseGiuseppe PiegariFrancesco PriscoIlaria CimminoClaudio PirozziGiuseppina Mattace RasoFrancesco OrienteEdoardo GriecoSerenella PapparellaOrlando PacielloPublished in: Journal of cellular physiology (2020)
NLRP3 inflammasome is a multiprotein complex that can sense several stimuli such as autophagy dysregulation and increased reactive oxygen species production stimulating inflammation by priming the maturation of proinflammatory cytokines interleukin-1β and interleukin-18 in their active form. In the aging brain, these cytokines can mediate the innate immunity response priming microglial activation. Here, we describe the results of immunohistochemical and molecular analysis carried out on bovine brains. Our results support the hypothesis that the age-related impairment in cellular housekeeping mechanisms and the increased oxidative stress can trigger the inflammatory danger sensor NLRP3. Moreover, according to the recent scientific literature, we demonstrate the presence of an age-related proinflammatory environment in aged brains consisting in an upregulation of interleukin-1β, an increased microglial activation and increased NLRP3 expression. Finally, we suggest that bovine may potentially be a pivotal animal model for brain aging studies.
Keyphrases
- nlrp inflammasome
- oxidative stress
- lipopolysaccharide induced
- poor prognosis
- reactive oxygen species
- lps induced
- resting state
- signaling pathway
- cell death
- inflammatory response
- white matter
- endoplasmic reticulum stress
- dna damage
- induced apoptosis
- cerebral ischemia
- ischemia reperfusion injury
- diabetic rats
- systematic review
- neuropathic pain
- traumatic brain injury
- functional connectivity
- spinal cord injury
- long non coding rna
- blood brain barrier
- subarachnoid hemorrhage