Exaggerated NLRP3 and IL-1β expression in <i>Vsig4<sup>-/-</sup></i> mice is accountable for deleterious disease severity in experimental autoimmune encephalomyelitis (EAE) and resistance to dextran sulfate sodium (DSS)-induced colitis.
In the present study, we have investigated the NLRP3 gain-of-function in the context of encephalomyelitis autoimmune disease (EAE), considered to be a Th1- and Th17-mediated disease.
Furthermore, administration of OL-CM reduced the expression of pro-inflammatory cytokines and suppressed the activation of NLRP3-inflammasome complex in EAE mice.
In this study, we evaluated the effects of TMP on the inflammatory response in experimental autoimmune encephalomyelitis (EAE), which is an animal model of MS. TMP (30 mg/kg) treatment significantly reduced the expression levels of NLR Family, Pyrin Domain-Containing 3 Protein inflammasome and caspase-1and decreased inflammatory infiltration and glial activation.
PNU282987 also significantly inhibited the activation of NLRP3 inflammasome and thus decreased the production of IL-1β and IL-18 both in lipopolysaccharide (LPS)/ATP-stimulated BV2 microglia in vitro and spinal cord from EAE mice in vivo, while inverse effects were observed in α7nAChR knockout mice.
We propose that the immunosuppressive role of hPDLSCs-derived conditioned medium and EMVs in EAE mice may partly attribute to the presence of soluble immunomodulatory factors, NALP3 inflammasome inactivation, and NF-κB reduction.
For example, the NLR family, pyrin domain containing 3 (NLRP3) inflammasome, which is known to sense a wide variety of pathogens, can also change the course of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS).
Experiments with the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), specifically describe the NLRP3 inflammasome as critical and necessary to disease development.