Sa1835 NLRP3 Inflammasome Ameliorates Ulcerative Colitis via Shifting Immune System to Th1

Itani, Shigehiro; Watanabe, Toshio; Nadatani, Yuji; Sugimura, Naoki; Shimada, Sunao; Takeda, Shogo; Otani, Koji; Hosomi, Syuhei; Nagami, Yasuaki; Tanaka, Fumio; Kamata, Noriko; Yamagami, Hirokazu; Tanigawa, Tetsuya; Shiba, Masatsugu; Tominaga, Kazunari; Fujiwara, Yasuhiro

doi:10.1016/s0016-5085(16)31324-5

Cited by 2 publications

(2 citation statements)

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“…Indeed, NLRP3 inflammasome activation may contribute to beneficial hostresponses directed against the virus as well as detrimental effects by causing hyperinflammation [9]. The NLRP3 inflammasome may also protect against colitis, for example through the effects of IL-18 which may induce MUC2 mucin expression [42].…”

Section: Nlrp3 Snvs Sickness Behavior and Covid-19mentioning

confidence: 99%

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

Maes

Tedesco

Lozovoy

et al. 2021

Preprint

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Background: In COVID-19, the NLRP3 inflammasome is activated in response to SARS-CoV-2 infection. Acute infections are accompanied by a sickness symptom complex (SSC) which is a highly conserved symptom complex that protects against infections and hyperinflammation. Aims: To examine the associations of COVID-19, SSC and the NLPR3 rs10157379 T>C and NLPR3 rs10754558 C>G SNV variants; and the protective role of SSC in severe acute respiratory syndrome (SARS)-CoV-2 infection. Methods: We recruited COVID-19 patients, 308 with critical, 63 with moderate and 157 with mild disease. Results: Increased SSC protects against SARS, critical disease, and death due to COVID-19. Increasing age, male sex and rs10754558 CG significantly predict reduced SSC protection. The rs10157379 CT and rs10754558 GG genotypes are positively associated with SARS. Partial Least Squares analysis shows a) that 41.8% of the variance in critical COVID-19 symptoms could be explained by SSC and oxygen saturation (inversely associated), and inflammation, chest computed tomography abnormalities, increased body mass index, SARS and age (positively associated); and b) the effects of the NLRP3 rs10157379 and rs10754558 variants on critical COVID-19 are mediated via SSC (protective) and SARS (detrimental). SSC includes anosmia, dysgeusia and gastrointestinal symptoms. Conclusions: Intersections among the rs10754558 variant, age, and sex increase risk towards critical COVID-19 by attenuating SSC. NLRP3 variants play an important role in SARS, and severe and critical COVID-19 especially in individuals with reduced SSC, elderly people, and those with increased BMI, hypertension, and diabetes type 2. SSC is a new drug target to combat acute COVID-19.

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Section: Nlrp3 Snvs Sickness Behavior and Covid-19mentioning

confidence: 99%

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

Maes

Tedesco

Lozovoy

et al. 2021

Preprint

View full text Add to dashboard Cite

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“…The inflammatory mediators regulated inflammatory pathways including nuclear factor kappa B (NF-κB) and mitogenactivated protein kinases (MAPKs; Zhu et al, 2018). A recent study found that the NLRP3 inflammasome also played a major role in the occurrence of UC (Itani et al, 2016). NLRP3 inflammasome activation was increased by the production of TNF-α and IL-1β and also induced apoptosis-related factors, which promoted intestinal epithelial cell pyroptosis.…”

Section: Introductionmentioning

confidence: 99%

The protective effect of nigeglanine on dextran sulfate sodium‐induced experimental colitis in mice and Caco‐2 cells

Gao

Tang

Liang

et al. 2019

Journal Cellular Physiology

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Ulcerative colitis (UC) was a nonspecific inflammatory disease. The treatment of UC is imperative. The present study aimed to investigate the effect of nigeglanine on dextran sulfate sodium-induced UC in experimental mice and Caco-2 cells and define the underlying mechanism. The nigeglanine was shown a significant protective effect on the colon, significantly reduced the weight and colon length loss and inhibited intestinal epithelial cell damage. Nigeglanine also reduced proinflammatory factors and increased anti-inflammatory factor production. The results indicate that nigeglanine suppresses the nuclear factor kappa B and mitogen-activated protein kinases pathways in addition to NLRP3 inflammasome action, inhibiting colon epithelial cell pyroptosis. Surprisingly, ZO-1 and occludin protein levels increased with nigeglanine treatment, suggesting that nigeglanine plays a protective role in barrier integrity, reducing colitis progression. The present study suggests that dietary therapy with nigeglanine may be a useful treatment for prophylaxis and palliative UC. K E Y W O R D Sdietary therapy, inflammatory factor, nigeglanine, NLRP3 inflammasome, ulcerative colitis

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Sa1835 NLRP3 Inflammasome Ameliorates Ulcerative Colitis via Shifting Immune System to Th1

Cited by 2 publications

References 0 publications

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

In COVID-19, NLRP3 inflammasome genetic variants are associated with critical disease and these effects are partly mediated by the sickness symptom complex: a nomothetic network approach

The protective effect of nigeglanine on dextran sulfate sodium‐induced experimental colitis in mice and Caco‐2 cells

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