Activation of NLRP3 Inflammasome in Inflammatory Bowel Disease: Differences Between Crohn’s Disease and Ulcerative Colitis

Lazaridis, Lazaros-Dimitrios; Pistiki, Aikaterini; Giamarellos‐Bourboulis, Evangelos J.; Georgitsi, Marianna; Damoraki, Georgia; Polymeros, Dimitrios; Dimitriadis, George; Triantafyllou, Konstantinos

doi:10.1007/s10620-017-4609-8

Cited by 86 publications

(62 citation statements)

References 24 publications

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“…Regarding the expression of NF-jB signalling molecules, these results are similar to previous studies [7][8][9], demonstrating an increase in expression of NF-rB and TNFa in OLP. Moreover, increased levels of NLRP3 inflammasome (NLRP3, ASC, caspase-1 and IL-1b) in OLP are in agreement with previous studies in other chronic inflammatory diseases [19][20][21]36]. Correlations between NF-rB signalling and NLRP3 inflammasome activation have been described in some studies [22,37].…”

Section: Discussionsupporting

confidence: 91%

“…In addition, NLRP3 inflammasome is associated with an inflammatory form of programmed cell death known as pyroptosis [17]. Increased expression of NLRP3 inflammasomes was observed in a variety of chronic inflammatory diseases, such as Crohn's disease [19] and periodontal diseases [20,21], upon activation of the NF-rB signalling pathway [22,23]. In addition, dysregulated inflammasome-mediated expression of cytokines such as IL-1b was reported to be associated with autoinflammatory diseases [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

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New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Thi

Phoomak

Champattanachai

et al. 2018

Clinical and Experimental Immunology

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Oral lichen planus (OLP) is considered a chronic inflammatory immune-mediated disease of the oral mucosa. Immunopathogenesis of OLP is thought to be associated with cell-mediated immune dysregulation. O-GlcNAcylation is a form of reversible glycosylation. It has been demonstrated that O-GlcNAcylation promoted nuclear factor kappa B (NF-κB) signalling. Activation of NF-кB can induce expression of nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is a large intracellular multi-protein complex involving an immune response. Dysregulated expression of the NLRP3 inflammasome was reported to be associated with autoinflammatory diseases. No integrative studies between O-GlcNAcylation and NLRP3 inflammasome in OLP patients have been reported. The present study aimed to determine the immunohistochemical expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome in oral mucosae of OLP patients. Oral tissue samples were collected from 30 OLP patients and 30 healthy individuals. Immunohistochemical staining and analyses of immunostaining scores were performed to evaluate expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome. According to observations in this study, significantly higher levels of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were demonstrated in OLP patients compared with control subjects (P < 0·001). Positive correlations among O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were also observed in OLP samples (P < 0·01). In conclusion, the present study provides supportive evidence that increased O-GlcNAcylation is associated with increased expression of NLRP3 inflammasome via the NF-κB signalling pathway. These findings provide a new perspective on immunopathogenesis of OLP in relation to autoinflammation.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Thi

Phoomak

Champattanachai

et al. 2018

Clinical and Experimental Immunology

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show abstract

“…Moreover, inhibition of the NLRP3 inflammasome with glyburide effectively suppressed the release of major proinflammatory cytokines/ chemokines by cultured colonic mucosal explants obtained from Crohn's patients [3]. These data support the hypothesis that the NLRP3 inflammasome contributes toward the pathogenesis of CD, a conclusion supported by the data reported by Lazaridis et al [10].…”

Section: Nlrp3 Inflammasomes and Ibdsupporting

confidence: 85%

“…Although this study by Lazaridis et al [10] appears to be straightforward and most of the results (such as associations of NLRP3 inflammasome activation with disease characteristics or ATG16L1 SNPs) appear to be negative, it is one of the few such reports using patient-derived cells or tissues. Currently, most of the reports on NLRP3 inflammasome are based on murine models of colitis.…”

Section: Nlrp3 Inflammasomes and Ibdmentioning

confidence: 87%

NLRP3 Inflammasome in Inflammatory Bowel Disease: Friend or Foe?

Liu

2017

Dig Dis Sci

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“…As a common malignant, colon cancer is a common malignancy, which ranks third in total morbidity and mortalities (2814,000) in the USA in 2015 (18). In China, colon cancer is the third most common cancer and ranks fifth for its mortality rate (19).…”

Section: Discussionmentioning

confidence: 99%

miRNA‑29a inhibits colon cancer growth by regulation of the PTEN/Akt/GSK3β and Wnt/β‑catenin signaling pathways

et al. 2018

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Abstract. In the present study, the effects of microRNA-29a (miRNA-29a) on colon cancer cell viability and the molecular mechanisms underlying the effects were investigated. The expression of miRNA-29a in colon cancer serum samples was notably downregulated, compared with in the normal group. First, miRNA-29a mimic was used to increase the expression of miRNA-29a in HCT-116 cells. Furthermore, upregulation of miRNA-29a suppressed cell viability, increased lactate dehydrogenase levels and apoptosis, and promoted caspase-3/9 activities and B-cell lymphoma 2-associated X protein and phosphatase and tensin homolog (PTEN) protein expression in colon cancer cells. Furthermore, upregulation of miRNA-29a decreased phosphoinositide 3-kinase, phosphorylated (p)-protein kinase B (Akt) and p-glycogen synthase kinase 3β (GSK3β) protein expression and suppressed the Wnt/β-catenin signaling pathway in colon cancer cells. The results of the present study verified that the protective effects of miRNA-29a suppress the PTEN/Akt/GSK3β and Wnt/β-catenin signaling pathways in colon cancer.

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Activation of NLRP3 Inflammasome in Inflammatory Bowel Disease: Differences Between Crohn’s Disease and Ulcerative Colitis

Abstract: NLRP3 inflammasome is activated in CD patients and in UC patients with long-standing disease.

Cited by 86 publications

References 24 publications

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

NLRP3 Inflammasome in Inflammatory Bowel Disease: Friend or Foe?

miRNA‑29a inhibits colon cancer growth by regulation of the PTEN/Akt/GSK3β and Wnt/β‑catenin signaling pathways

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