NLRP3 Inflammasome in Inflammatory Bowel Disease: Friend or Foe?

Liu, Ling; Li, Xuhang

doi:10.1007/s10620-017-4650-7

Cited by 10 publications

(3 citation statements)

References 12 publications

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“…Multiple pathogen-related molecular patterns (PAMPs), riskrelated molecular patterns (DAMPs) and environmental stimuli can activate NLRP3 inflammatory bodies (12). After the NLRP3 scaffold protein is activated, NLRP3 monomers achieve oligomerization through NACHT (NAIP, CIITA, HET-E and TP1) domain interactions (13). In turn, the PYD (pyrin domain) domain of NLRP3 is exposed to interact with the PYD domain of ASC, which promotes the self-activation of caspase-1 and Caspase-1 before recruitment by the CARD (caspase recruitment domain) domain of ASC and cleave the pro-inflammatory factors IL-1B and IL-18.…”

Section: Curcumin Reduces Psoriasis-like Skin Lesions In Mice By Inhi...mentioning

confidence: 99%

Curcumin reduces inflammation in mice with the psoriasis model by inhibiting NLRP3 inflammatory bodies

Zhang¹,

2022

Cell Mol Biol (Noisy-le-grand)

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As a chronic skin disease, psoriasis is a relatively common disease among various types of skin diseases. Because this disease is often distributed throughout the patient's body and is prone to develop, it is difficult to guarantee the quality of life and physical and mental health of patients with this disease. The purpose of this article is to investigate whether curcumin can effectively inhibit the NLRP3 inflammatory body and thereby reduce the inflammation in the mouse psoriasis model. Through the use of the curcumin gel prepared and the mouse psoriasis model, the percutaneous administration was used to investigate the mechanism and mechanism of curcumin's effect on reducing inflammation in the mouse psoriasis model. In addition, in order to better explore the curative effect of curcumin on psoriasis, related experiments were conducted by setting up a control group and an experimental group. The results show that curcumin has a good inhibitory effect on NLRP3 inflammatory bodies. Curcumin can not only reduce the NLRP3 expression and inhibit the inflammation caused by IL-22 and IL-18 but also reduce the damage of psoriasis. 22 Induced phosphorylation of STAT3 almost completely inhibits phosphorylation in normal cells. Among them, curcumin inhibited IL-22-induced phosphorylation of STAT3 up to 95.6%, and inhibited IL-22 and IL-18 by about 47%.

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Section: Curcumin Reduces Psoriasis-like Skin Lesions In Mice By Inhi...mentioning

confidence: 99%

Curcumin reduces inflammation in mice with the psoriasis model by inhibiting NLRP3 inflammatory bodies

Zhang¹,

2022

Cell Mol Biol (Noisy-le-grand)

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“…Over-expression and activation of NLRC4, NLRP1, AIM2 and NLRP3 inflammasome [25][26][27] Type 1 Diabetes Pancreas Over-expression NLRP1, NOD1/2, CIITA and NLRP3 [26,28,29] Inflammatory bowel diseases (IBD: Ulcerative colitis and Crohn's disease) Gastrointestinal NOD1, NOD2, NLRP3 and NLRP1 [26,[30][31][32][33] Celiac diseases Small intestine Enhanced expression of NLRP3 and CIITA, NLRP6 [26,29,34] NOD2, NLRC5 and NLRP12 (beneficial), and NLRP9 and NLRP11 [25,26,[37][38][39][40] Systemic Lupus Erythematous (SLE)…”

Section: Thyroiditis Thyroid Glandmentioning

confidence: 99%

Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections

Babamale

Chen

2021

IJMS

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Cell death is an essential immunological apparatus of host defense, but dysregulation of mutually inclusive cell deaths poses severe threats during microbial and parasitic infections leading to deleterious consequences in the pathological progression of infectious diseases. Nucleotide-binding oligomerization domain (NOD)-Leucine-rich repeats (LRR)-containing receptors (NLRs), also called nucleotide-binding oligomerization (NOD)-like receptors (NLRs), are major cytosolic pattern recognition receptors (PRRs), their involvement in the orchestration of innate immunity and host defense against bacteria, viruses, fungi and parasites, often results in the cleavage of gasdermin and the release of IL-1β and IL-18, should be tightly regulated. NLRs are functionally diverse and tissue-specific PRRs expressed by both immune and non-immune cells. Beyond the inflammasome activation, NLRs are also involved in NF-κB and MAPK activation signaling, the regulation of type I IFN (IFN-I) production and the inflammatory cell death during microbial infections. Recent advancements of NLRs biology revealed its possible interplay with pyroptotic cell death and inflammatory mediators, such as caspase 1, caspase 11, IFN-I and GSDMD. This review provides the most updated information that caspase 8 skews the NLRP3 inflammasome activation in PANoptosis during pathogen infection. We also update multidimensional roles of NLRP12 in regulating innate immunity in a content-dependent manner: novel interference of NLRP12 on TLRs and NOD derived-signaling cascade, and the recently unveiled regulatory property of NLRP12 in production of type I IFN. Future prospects of exploring NLRs in controlling cell death during parasitic and microbial infection were highlighted.

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“…The innate immune system provides the first line of the host defense against pathogenic microbes and also plays an important role in regulating the immune homeostasis of the intestine [10][11][12]. As a major arm of innate immunity, the inflammasomes are considered to be prominent factors in modulating the development of inflammatory responses in the gut [13,14]. Mounting recent evidence shows that inflammasomes might have the potential to be a therapeutic target for treatment of IBD.…”

Section: Introduction 1inflammatory Bowel Diseasementioning

confidence: 99%

Inflammasome Regulation: Therapeutic Potential for Inflammatory Bowel Disease

Zhou

Strober

et al. 2021

Molecules

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Inflammasomes are multiprotein complexes formed to regulate the maturation of pro-inflammatory caspases, in response to intracellular or extracellular stimulants. Accumulating studies showed that the inflammasomes are implicated in the pathogenesis of inflammatory bowel disease (IBD), although their activation is not a decisive factor for the development of IBD. Inflammasomes and related cytokines play an important role in the maintenance of gut immune homeostasis, while its overactivation might induce excess immune responses and consequently cause tissue damage in the gut. Emerging studies provide evidence that some genetic abnormalities might induce enhanced NLRP3 inflammasome activation and cause colitis. In these cases, the colonic inflammation can be ameliorated by blocking NLRP3 activation or its downstream cytokine IL-1β. A number of natural products were shown to play a role in preventing colon inflammation in various experimental colitis models. On the other hand, lack of inflammasome function also causes intestinal abnormalities. Thus, an appropriate regulation of inflammasomes might be a promising therapeutic strategy for IBD intervention. This review aims at summarizing the main findings in these studies and provide an outline for further studies that might contribute to our understanding of the role of inflammasomes in the pathogenesis and therapeutic treatment of IBD.

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NLRP3 Inflammasome in Inflammatory Bowel Disease: Friend or Foe?

Cited by 10 publications

References 12 publications

Curcumin reduces inflammation in mice with the psoriasis model by inhibiting NLRP3 inflammatory bodies

Curcumin reduces inflammation in mice with the psoriasis model by inhibiting NLRP3 inflammatory bodies

Nod-like Receptors: Critical Intracellular Sensors for Host Protection and Cell Death in Microbial and Parasitic Infections

Inflammasome Regulation: Therapeutic Potential for Inflammatory Bowel Disease

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