<scp>NLRP</scp>3 inflammasome: A likely target for the treatment of allergic diseases

Xiao, Yunfeng; Xu, W.; Su, Wenru

doi:10.1111/cea.13190

Cited by 59 publications

(55 citation statements)

References 128 publications

(142 reference statements)

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“…Classical studies show that activation of NLRP3 inflammasome consists of initial priming which upregulates the components of inflammasome, and then activation signal that promoting the assembly of inflammasome and the formation of persistent chronic inflammation . In our study, both LPS + CTPE and CTPE exposure promoted the expression of NLRP3 and the combination of NLRP3 and caspase‐1, indicating the important role of NLRP3 inflammasome in the transformation of LPS + CTPE‐ or CTPE‐induced BEAS‐2B cells . Moreover, we found that LPS + CTPE exposure upregulated the mRNA and protein levels of NLRP3 in comparison to the cells exposed to LPS or CTPE.…”

Section: Discussionsupporting

confidence: 68%

NLRP3 inflammasome activation involved in LPS and coal tar pitch extract‐induced malignant transformation of human bronchial epithelial cells

Duan

Wang

Huang

et al. 2019

Environmental Toxicology

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Inflammatory microenvironment has been found as a new characteristic of cancer; however, the mechanisms of inflammation-related lung cancer remain unclear. To explore the role of NLRP3 inflammsome activation in inflammation-related lung carcinogenesis, a cell model was set up. Human bronchial epithelial cells (BEAS-2B) were stimulated with 1 μg/mL lipopolysaccharide (LPS) for 24 hours, and then treated with 2.4 μg/mL coal tar pitch extract (CTPE) for 24 hours, after removal of LPS and CTPE, the cells were numbered passage 1 and were passaged and treated in this way until passage 30, which was called LPS + CTPE group. DMSO and Saline were used as vehicle controls. Malignant transformation of cells in passage 30 was evaluated by morphological change, platelet clone formation assay, and tumor formation in nude mice. The mRNA levels of NLRP3 and IL-1β were detected by real time-PCR. The combination of NLRP3 and caspase-1 were determined using immunofluorescence and confocal. The protein expression of NLRP3, cleaved caspase-1(p10), and cleaved IL-1β was detected using Western blot. It was shown that CTPE, LPS + CTPEstimulated BEAS-2B cells of passage 30 changed a lot morphologically. The clone formation rates, the rates of positive cells of NLRP3 and caspase-1 combination, the mRNA levels of NLRP3 and IL-1β, the protein expression of NLRP3, cleaved caspase-1(p10) and cleaved IL-1β of cells exposed with CTPE and LPS + CTPE at passage 30 were significantly increased compared to vehicle controls. Furthermore, the ability of tumor formation in nude mice, the rates of clone formation and positive cells, mRNA and protein levels of NLRP3 inflammasome activation-related factors in LPS + CTPE-induced cells were all higher than those in cells stimulated with CTPE alone. In conclusion, the cell model of inflammation-related lung cancer is set up successfully, and NLRP3 inflammasome activation may be involved in the malignant transformation of BEAS-2B cells which induced by CTPE alone or LPS combined with CTPE.

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Section: Discussionsupporting

confidence: 68%

NLRP3 inflammasome activation involved in LPS and coal tar pitch extract‐induced malignant transformation of human bronchial epithelial cells

Duan

Wang

Huang

et al. 2019

Environmental Toxicology

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“…In addition to the Th2 response, a Th17 response is associated with asthma, notably severe glucocorticoid‐resistant asthma . From various studies of human diseases and mouse models, the elevation of IL‐1β and IL‐18 is associated with the development of allergic diseases, such as asthma, dermatitis, rhinitis, and conjunctivitis . All these events are connected with inflammasome activation and suggest participation of the inflammasome in the development and progression of asthma.…”

Section: Inflammasomementioning

confidence: 99%

Innate immunity in allergy

Maeda

Caldez

Akira

2019

Allergy

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Innate immune system quickly responds to invasion of microbes and foreign substances through the extracellular and intracellular sensing receptors, which recognize distinctive molecular and structural patterns. The recognition of innate immune receptors leads to the induction of inflammatory and adaptive immune responses by activating downstream signaling pathways. Allergy is an immune‐related disease and results from a hypersensitive immune response to harmless substances in the environment. However, less is known about the activation of innate immunity during exposure to allergens. New insights into the innate immune system by sensors and their signaling cascades provide us with more important clues and a framework for understanding allergy disorders. In this review, we will focus on recent advances in the innate immune sensing system.

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“…As a member of the cysteine-aspartic acid protease family, caspase-1 is activated through the cleavage of pro-caspase-1 (25). In response to allergens or associated molecular signals, the NLRP3 inflammasome complex will be assembled and activate caspase-1, which proteolytically cleaves other proteins including the precursor of IL-1β (26). Our investigation has unraveled irisflorentin can reduce the secretion of pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 in RBL-2H3 cells stimulated by DNP-HSA.…”

Section: Discussionmentioning

confidence: 80%

Irisflorentin suppresses allergic inflammation in mast cells via reducing histamine release and production of pro-inflammatory cytokines

Li¹,

Meng²

2019

Acta Poloniae Pharmaceutica - Drug Research

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Allergic diseases afflict many people worldwide. Allergic inflammation encompassing acute allergic reaction and chronic inflammatory response is the major pathogenesis. To discovery novel therapeutic approach for allergic diseases, we have evaluated the anti-allergic inflammatory effects of irisflorentin using RBL-2H3 cells. The results showed certain concentrations of irisflorentin could suppress histamine release and secretion of TNF-α, IL-1β and IL-6. Further investigations indicated that the effects of irisflorentin were associated with a reduction of intracellular calcium, suppression of NF-κB signaling pathway and inhibition of caspase-1 activity. Therefore, the results of the current study demonstrated that irisflorentin can ameliorate mast cell-mediated allergic inflammation. These results can provide evidence for the discovery of novel therapy for allergic diseases and application of irisflorentin in practice.

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NLRP3 inflammasome: A likely target for the treatment of allergic diseases

Cited by 59 publications

References 128 publications

NLRP3 inflammasome activation involved in LPS and coal tar pitch extract‐induced malignant transformation of human bronchial epithelial cells

NLRP3 inflammasome activation involved in LPS and coal tar pitch extract‐induced malignant transformation of human bronchial epithelial cells

Innate immunity in allergy

Irisflorentin suppresses allergic inflammation in mast cells via reducing histamine release and production of pro-inflammatory cytokines

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