Objectives: To investigate the role of NLRP3 and NLRP1 inflammasomes signaling pathways in rheumatoid arthritis (RA).
Methods: A total of 36 patients with RA were selected, peripheral blood mononuclear cell (PBMC) and granulocyte were separated from venous blood. RT-qPCR method was used to detect the expression level and diversity of NLRP3 and NLRP1 in PBMC and granulocyte mRNA in patients with RA, and detect the mRNA expression of downstream factor IL-1α. The correlation between RA and the expression of NLRP3 and NLRP1 was analyzed. Normal 30 cases were set as control group.
Results: Expression levels of NLRP1, and caspase-1 mRNA in PBMC of RA group were significantly lower than those of control group (P<0.05), while there was no significant difference in expression levels of NLRP3, ASC, IL-1α mRNA between these two groups (P>0.05); NLRP3, caspase-1, and ASC mRNA expression in granulocyte of RA patients were significantly lower than those in control group (P<0.05). There was no correlation between rheumatoid factor and expression levels of NLRP3, ASC, caspase-1 mRNA in RA group (P>0.05); NLRP1, IL-1α mRNA expression level had a negative correlation with anti-rheumatoid factor antibody (P=0.033 2, 0.034 0).
Conclusions: NLRP3 and NLRP1 inflammasomes signaling pathways are involved in RA inflammatory reaction process as protective factors, and play an important role in RA inflammatory mechanisms.
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http://dx.doi.org/10.1016/S1995-7645(14)60145-0 | DOI Listing |
Immunol Rev
January 2025
Department of Internal Medicine and Paediatrics, Ghent University, Ghent, Belgium.
Inflammasomes are crucial mediators of both antimicrobial host defense and inflammatory pathology, requiring stringent regulation at multiple levels. This review explores the pivotal role of mitogen-activated protein kinase (MAPK) signaling in modulating inflammasome activation through various regulatory mechanisms. We detail recent advances in understanding MAPK-mediated regulation of NLRP3 inflammasome priming, licensing and activation, with emphasis on MAPK-induced activator protein-1 (AP-1) signaling in NLRP3 priming, ERK1 and JNK in NLRP3 licensing, and TAK1 in connecting death receptor signaling to NLRP3 inflammasome activation.
View Article and Find Full Text PDFAn Acad Bras Cienc
December 2024
Universidade Federal de Pernambuco, Departamento de Medicina Tropical, Av. Prof. Moraes Rego, s/n, Cidade Universitária, 50670-420 Recife, PE, Brazil.
The COVID-19 pandemic has been the largest pandemic of the past century, and various genetic factors have played a significant role in this context. This study aimed to analyze the frequency and association between specific SNPs rs3806268 (NLRP3), rs4925543 (NLRP3), rs12150220 (NLRP1), rs455060 (NLRC4), rs699 (AGT), rs1137101 (LEPR), and rs1801133 (MTHFR) and severe/critical outcomes in Brazilian patients with COVID-19. A total of 100 patients were included in the study, comprising 66 cases and 34 controls.
View Article and Find Full Text PDFParasit Vectors
November 2024
School of Basic Medicine, Basic Medical Sciences Center, Shanxi Medical University, Jinzhong, 030600, Shanxi, China.
Background: The detection of pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) by multimeric protein complexes, known as inflammasomes, triggers an inflammatory response, which is a critical component of the innate immune system. This inflammatory response plays a pivotal role in host resistance against parasitic infections, presenting a significant global health challenge.
Methods: We systematically searched for relevant articles from the Pubmed and the Web of Science database to summarize current insights into how inflammasomes function in preventing infections caused by the apicomplexan parasites Toxoplasma and Plasmodium.
Immunol Invest
November 2024
Laboratório de Imunogenética, Departamento de Imunologia, Instituto de Ciências Biomédicas/ICB, Universidade de São Paulo/USP, São Paulo, Brazil.
Exp Eye Res
October 2023
Department of Ophthalmology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine (Key Laboratory for Corneal Diseases Research of Zhejiang Province), Hangzhou, Zhejiang, 310016, China. Electronic address:
The role and related mechanisms of tetramethylpyrazine (TMP) in corneal alkali burn in rats were expected to be explored in this article. After construction of corneal alkali burn rat models, TMP eye drops were given four times daily for consecutive 7 days. H&E staining was utilized for observing the histopathological changes of corneas on the 3rd and 7th days of treatment; immunohistochemistry for detecting the Nestin protein expression changes; qRT-PCR for determining the expression changes of genes correlated with neovascularization [C-X-C Motif Chemokine Ligand 1 (CXCL-1), vascular endothelial growth factor A (VEGFA) and CD31] and inflammation-related factors [monocyte chemoattractant protein-1 (MCP-1), interleukin-1β (IL-1β), tumour necrosis factor α (TNF-α), and IL-6]; Western blot for testing NLR Family Pyrin Domain Containing 1 (NLRP1)/NLRP3 inflammasomes and toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway-related protein expression changes.
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