Enteric glial NLRP3 inflammasome contributes to gut mucosal barrier alterations in a mouse model of diet-induced obesity.
Vanessa D'AntongiovanniMatteo FornaiRocchina ColucciAnna NericcioLaura BenvenutiClelia Di SalvoCristina SegnaniClarissa PierucciChiara IppolitoZoltan H NemethGyörgy HaskóNunzia BernardiniLuca AntonioliCarolina PellegriniPublished in: Acta physiologica (Oxford, England) (2024)
HFD intake elicits mucosal enteric gliotic processes characterized by a hyperactivation of NLRP3/caspase-1/IL-1β signaling pathway, that contributes to further exacerbate the disruption of intestinal mucosal barrier integrity. However, we cannot rule out the contribution of NLRP3 inflammasome activation from other cells, such as immune cells, in IEB alterations associated with obesity. Overall, our results suggest that enteric glial NLRP3 inflammasome might represent an interesting molecular target for the development of novel pharmacological approaches aimed at managing the enteric inflammation and intestinal mucosal dysfunctions associated with obesity.
Keyphrases
- nlrp inflammasome
- insulin resistance
- induced apoptosis
- metabolic syndrome
- weight loss
- weight gain
- ulcerative colitis
- high fat diet induced
- signaling pathway
- type diabetes
- mouse model
- oxidative stress
- high fat diet
- endoplasmic reticulum stress
- neuropathic pain
- cell death
- pi k akt
- adipose tissue
- skeletal muscle
- cell proliferation
- spinal cord
- physical activity