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Article ; Online: Microbial exposure during early life regulates development of bile duct inflammation.

Oldereid, Tine S / Jiang, Xiaojun / Øgaard, Jonas / Schrumpf, Elisabeth / Bjørnholt, Jørgen V / Rasmussen, Henrik / Melum, Espen

Scandinavian journal of gastroenterology

2024 Volume 59, Issue 2, Page(s) 192–201

Abstract: Objectives: The early life microbiome has been linked to inflammatory diseases in adulthood and a role for the microbiome in bile duct inflammation is supported by both human and murine studies. We utilized the NOD.c3c4 mouse model that develops a ... ...

Abstract	Objectives: The early life microbiome has been linked to inflammatory diseases in adulthood and a role for the microbiome in bile duct inflammation is supported by both human and murine studies. We utilized the NOD.c3c4 mouse model that develops a spontaneous immune-driven biliary disease with a known contribution of the microbiome to evaluate the temporal effects of the early life microbiome. Materials and methods: Germ-free (GF) NOD.c3c4 mice were conventionalized into a specific pathogen free environment at birth (conventionally raised, CONV-R) or at weaning (germ-free raised, GF-R) and compared with age and gender-matched GF and conventional (CONV) NOD.c3c4 mice. At 9 weeks of age, liver pathology was assessed by conventional histology and flow cytometry immunophenotyping. Results: Neonatal exposure to microbes (CONV-R) increased biliary inflammation to similar levels as regular conventional NOD.c3c4 mice, while delayed exposure to microbes (GF-R) restrained the biliary inflammation. Neutrophil infiltration was increased in all conventionalized mice compared to GF. An immunophenotype in the liver similar to CONV was restored in both CONV-R and GF-R compared to GF mice displaying a proportional increase of B cells and reduction of T cells in the liver. Conclusions: Microbial exposure during early life has a temporal impact on biliary tract inflammation in the NOD.c3c4 mouse model suggesting that age-sensitive interaction with commensal microbes have long-lasting effects on biliary immunity that can be of importance for human cholangiopathies.
MeSH term(s)	Mice ; Humans ; Animals ; Mice, Inbred NOD ; Cholangitis ; Liver/pathology ; Inflammation/pathology ; Disease Models, Animal ; Bile Ducts/pathology
Language	English
Publishing date	2024-01-30
Publishing country	England
Document type	Journal Article
ZDB-ID	82042-8
ISSN	1502-7708 ; 0036-5521
ISSN (online)	1502-7708
ISSN	0036-5521
DOI	10.1080/00365521.2023.2278423
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Article ; Online: Coaggregation properties of trimeric autotransporter adhesins.

Khalil, Hawzeen S / Øgaard, Jonas / Leo, Jack C

MicrobiologyOpen

2020 Volume 9, Issue 10, Page(s) e1109

Abstract: Trimeric autotransporter adhesins (TAAs) comprise a group of virulence-related proteins in Gram-negative bacteria. Members of this family bind to extracellular matrix components such as collagen and fibronectin, but also they exhibit several other ... ...

Abstract	Trimeric autotransporter adhesins (TAAs) comprise a group of virulence-related proteins in Gram-negative bacteria. Members of this family bind to extracellular matrix components such as collagen and fibronectin, but also they exhibit several other functions, such as conferring serum resistance and autoaggregation. Autoaggregation promoted by TAAs is homotypic and mediated by the sticky, globular head domains of these lollipop-like molecules. However, whether TAAs mediate heterotypic interactions (i.e., coaggregation) has not been studied. To address this question, we investigated the coaggregation of two model TAA groups: YadA from the enteropathogenic Yersiniae and the immunoglobulin-binding Eib proteins from Escherichia coli. To study TAA coaggregation, we coexpressed a fluorescent label together with a particular TAA and followed the aggregative interactions using fluorescence microscopy and quantified the interactions using a novel script implemented in Fiji. Our results show that there is coaggregation between some populations expressing different TAAs, which can be explained by relatively high sequence similarity between the interacting TAAs. Generally, the level of coaggregation correlated with the sequence similarity. However, some TAAs did not interact despite high sequence similarity, showing exclusion of bacteria producing a noncompatible TAA. These data demonstrate that TAAs can mediate bacterial coaggregation, but in some cases prevent coaggregation of bacteria with disparate TAAs. Our results have implications for the ecology of TAA-producing bacteria, where coaggregation may promote co-operation whereas exclusion might be an indication of competition.
MeSH term(s)	Adhesins, Bacterial/chemistry ; Adhesins, Bacterial/genetics ; Adhesins, Bacterial/metabolism ; Biofilms ; Escherichia coli/chemistry ; Escherichia coli/genetics ; Escherichia coli/growth & development ; Escherichia coli/metabolism ; Escherichia coli Proteins/chemistry ; Escherichia coli Proteins/genetics ; Escherichia coli Proteins/metabolism ; Protein Conformation
Chemical Substances	Adhesins, Bacterial ; Escherichia coli Proteins
Language	English
Publishing date	2020-08-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661368-2
ISSN	2045-8827 ; 2045-8827
ISSN (online)	2045-8827
ISSN	2045-8827
DOI	10.1002/mbo3.1109
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Article ; Online: Spatial transcriptomics identifies enriched gene expression and cell types in human liver fibrosis.

Chung, Brian K / Øgaard, Jonas / Reims, Henrik Mikael / Karlsen, Tom H / Melum, Espen

Hepatology communications

2022 Volume 6, Issue 9, Page(s) 2538–2550

Abstract: Liver fibrosis and cirrhosis have limited therapeutic options and represent a serious unmet patient need. Recent use of single-cell RNA sequencing (scRNAseq) has identified enriched cell types infiltrating cirrhotic livers but without defining the ... ...

Abstract	Liver fibrosis and cirrhosis have limited therapeutic options and represent a serious unmet patient need. Recent use of single-cell RNA sequencing (scRNAseq) has identified enriched cell types infiltrating cirrhotic livers but without defining the microanatomical location of these lineages thoroughly. To assess whether fibrotic liver regions specifically harbor enriched cell types, we explored whether whole-tissue spatial transcriptomics combined with scRNAseq and gene deconvolution analysis could be used to localize cell types in cirrhotic explants of patients with end-stage liver disease (total n = 8; primary sclerosing cholangitis, n = 4; primary biliary cholangitis, n = 2, alcohol-related liver disease, n = 2). Spatial transcriptomics clearly identified tissue areas of distinct gene expression that strongly correlated with the total area (Spearman r = 0.97, p = 0.0004) and precise location (parenchyma, 87.9% mean congruency; range, 73.1%-97.1%; fibrosis, 68.5% mean congruency; range, 41.0%-91.7%) of liver regions classified as parenchymal or fibrotic by conventional histology. Deconvolution and enumeration of parenchymal and fibrotic gene content as measured by spatial transcriptomics into distinct cell states revealed significantly higher frequencies of ACTA2+ FABP4+ and COL3A1+ mesenchymal cells, IL17RA+ S100A8+ and FCER1G+ tissue monocytes, VCAM1+ SDC3+ Kupffer cells, CCL4+ CCL5+ KLRB1+ and GZMA+ IL17RA+ T cells and HLA-DR+, CD37+ CXCR4+ and IGHM+ IGHG+ B cells in fibrotic liver regions compared with parenchymal areas of cirrhotic explants. Conclusion: Our findings indicate that spatial transcriptomes of parenchymal and fibrotic liver regions express unique gene content within cirrhotic liver and demonstrate proof of concept that spatial transcriptomes combined with additional RNA sequencing methodologies can refine the localization of gene content and cell lineages in the search for antifibrotic targets.
MeSH term(s)	Fibrosis ; Humans ; Liver Cirrhosis/genetics ; Liver Diseases ; Transcriptome/genetics
Language	English
Publishing date	2022-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1002/hep4.2001
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Article ; Online: SLAMF1-derived peptide exhibits cardio protection after permanent left anterior descending artery ligation in mice.

Olsen, Maria Belland / Kong, Xiang Yi / Louwe, Mieke C / Lauritzen, Knut H / Schanke, Ylva / Kaasbøll, Ole Jørgen / Attramadal, Håvard / Øgaard, Jonas / Holm, Sverre / Aukrust, Pål / Ryan, Liv / Espevik, Terje / Yurchenko, Maria / Halvorsen, Bente

Frontiers in immunology

2024 Volume 15, Page(s) 1383505

Abstract: Acute myocardial infarction (MI) results in tissue damage to affected areas of the myocardium. The initial inflammatory response is the most damaging for residual cardiac function, while at later stages inflammation is a prerequisite for proper healing ... ...

Abstract	Acute myocardial infarction (MI) results in tissue damage to affected areas of the myocardium. The initial inflammatory response is the most damaging for residual cardiac function, while at later stages inflammation is a prerequisite for proper healing and scar formation. Balancing the extent and duration of inflammation during various stages after MI is thus pivotal for preserving cardiac function. Recently, a signaling lymphocytic activation molecule 1 (SLAMF1)-derived peptide (P7) was shown to reduce the secretion of inflammatory cytokines and protected against acute lipopolysaccharide-induced death in mice. In the present study, we experimentally induced MI by permanent ligation of the left anterior descending artery (LAD) in mice and explored the beneficial effect of immediately administering P7, with the aim of dampening the initial inflammatory phase without compromising the healing and remodeling phase. Blood samples taken 9 h post-LAD surgery and P7 administration dampened the secretion of inflammatory cytokines, but this dampening effect of P7 was diminished after 3 days. Echocardiography revealed less deterioration of cardiac contraction in mice receiving P7. In line with this, less myocardial damage was observed histologically in P7-treated mice. In conclusion, the administration of a SLAMF1-derived peptide (P7) immediately after induction of MI reduces the initial myocardial inflammation, reduces infarct expansion, and leads to less deterioration of cardiac contraction.
MeSH term(s)	Animals ; Mice ; Myocardial Infarction ; Male ; Disease Models, Animal ; Cytokines/metabolism ; Mice, Inbred C57BL ; Antigens, CD/metabolism ; Ligation ; Myocardium/pathology ; Myocardium/metabolism ; Peptides/pharmacology ; Receptors, Cell Surface/metabolism ; Coronary Vessels/drug effects ; Coronary Vessels/pathology
Chemical Substances	Cytokines ; Antigens, CD ; Ly78 protein, mouse ; Peptides ; Receptors, Cell Surface
Language	English
Publishing date	2024-04-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2024.1383505
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Article ; Online: Bile from Patients with Primary Sclerosing Cholangitis Contains Mucosal-Associated Invariant T-Cell Antigens.

Valestrand, Laura / Zheng, Fei / Hansen, Simen H / Øgaard, Jonas / Hov, Johannes R / Björkström, Niklas K / Karlsen, Tom H / Jiang, Xiaojun / Melum, Espen

The American journal of pathology

2022 Volume 192, Issue 4, Page(s) 629–641

Abstract: Primary sclerosing cholangitis (PSC) is associated with altered microbiota of the gut and bile. Mucosal-associated invariant T (MAIT) cells, enriched in human liver, uniquely recognize microbial-derived metabolites. This study aimed to determine whether ... ...

Abstract	Primary sclerosing cholangitis (PSC) is associated with altered microbiota of the gut and bile. Mucosal-associated invariant T (MAIT) cells, enriched in human liver, uniquely recognize microbial-derived metabolites. This study aimed to determine whether bile from patients with PSC contains antigens activating MAIT cells. Bile was collected at the time of liver transplantation from patients with PSC (n = 28). The bile samples were either directly incubated with peripheral blood mononuclear cells from healthy donors or with antigen-presenting cells followed by co-culture with peripheral blood mononuclear cells. MAIT cell activation was assessed by flow cytometry. An anti-MR1 antibody was used to determine whether the activation was major histocompatibility complex class I-related protein (MR1) restricted. Biliary microbiota profiles were generated using 16S rRNA amplicon sequencing, and the abundance of the bacterial gene ribD was predicted. Eight of 28 bile samples could activate MAIT cells. This activation was partly MR1-dependent in five of eight bile samples. Microbial DNA was detected in 15 of 28 bile samples, including the five bile samples leading to MR1-dependent activation. A higher abundance of the ribD gene expression in the group of bile samples that could activate MAIT cells was predicted on the basis of the 16S sequencing. In co-culture experiments, cholangiocytes could take up and present biliary antigens to MAIT cells. These findings suggest a pathophysiological pathway in PSC connecting the immune system and the microbiome.
MeSH term(s)	Antigens ; Bile/metabolism ; Cholangitis, Sclerosing ; Histocompatibility Antigens Class I/genetics ; Histocompatibility Antigens Class I/metabolism ; Humans ; Leukocytes, Mononuclear/metabolism ; Mucosal-Associated Invariant T Cells ; RNA, Ribosomal, 16S
Chemical Substances	Antigens ; Histocompatibility Antigens Class I ; RNA, Ribosomal, 16S
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2021.12.008
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Article ; Online: Cholangiocytes Modulate CD100 Expression in the Liver and Facilitate Pathogenic T-Helper 17 Cell Differentiation.

Jiang, Xiaojun / Otterdal, Kari / Chung, Brian K / Maucourant, Christopher / Rønneberg, Jørgen D / Zimmer, Christine L / Øgaard, Jonas / Boichuk, Yuliia / Holm, Sverre / Geanon, Daniel / Schneditz, Georg / Bergquist, Annika / Björkström, Niklas K / Melum, Espen

Gastroenterology

2023 Volume 166, Issue 4, Page(s) 667–679

Abstract: Background & aims: Chronic inflammation surrounding bile ducts contributes to the disease pathogenesis of most cholangiopathies. Poor efficacy of immunosuppression in these conditions suggests biliary-specific pathologic principles. Here we performed ... ...

Abstract	Background & aims: Chronic inflammation surrounding bile ducts contributes to the disease pathogenesis of most cholangiopathies. Poor efficacy of immunosuppression in these conditions suggests biliary-specific pathologic principles. Here we performed biliary niche specific functional interpretation of a causal mutation (CD100 K849T) of primary sclerosing cholangitis (PSC) to understand related pathogenic mechanisms. Methods: Biopsy specimens of explanted livers and endoscopy-guided sampling were used to assess the CD100 expression by spatial transcriptomics, immune imaging, and high-dimensional flow cytometry. To model pathogenic cholangiocyte-immune cell interaction, splenocytes from mutation-specific mice were cocultured with cholangiocytes. Pathogenic pathways were pinpointed by RNA sequencing analysis of cocultured cells and cross-validated in patient materials. Results: CD100 is mainly expressed by immune cells in the liver and shows a unique pattern around PSC bile ducts with RNA-level colocalization but poor detection at the protein level. This appears to be due to CD100 cleavage as soluble CD100 is increased. Immunophenotyping suggests biliary-infiltrating T cells as the major source of soluble CD100, which is further supported by reduced surface CD100 on T cells and increased metalloproteinases in cholangiocytes after coculturing. Pathogenic T cells that adhered to cholangiocytes up-regulated genes in the T-helper 17 cell differentiation pathway, and the CD100 mutation boosted this process. Consistently, T-helper 17 cells dominate biliary-resident CD4 T cells in patients. Conclusions: CD100 exerts its functional impact through cholangiocyte-immune cell cross talk and underscores an active, proinflammatory role of cholangiocytes that can be relevant to novel treatment approaches.
MeSH term(s)	Humans ; Animals ; Mice ; Liver/pathology ; Bile Ducts/pathology ; Biliary Tract/pathology ; Epithelial Cells/pathology ; Cholangitis ; Cell Differentiation ; Cholangitis, Sclerosing/pathology
Language	English
Publishing date	2023-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	80112-4
ISSN	1528-0012 ; 0016-5085
ISSN (online)	1528-0012
ISSN	0016-5085
DOI	10.1053/j.gastro.2023.11.283
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Article ; Online: T cells with increased responsiveness cause obesity in mice without diet intervention.

Gregersen, Ida / Kong, Xiang Y / Kooijman, Sander / Foyn, Håvard / Grannes, Helene / Olsen, Maria B / Lone, Anna M / Yang, Kuan / Quiles-Jiménez, Ana / Tran, Marianne / Øgaard, Jonas / Segers, Filip M / Rashidi, Azita / Sagen, Ellen Lund / Lauritzen, Knut H / Pronk, Amanda C M / de Boer, Jan Freark / Holven, Kirsten B / Melum, Espen /

Aukrust, Pål / Taskén, Kjetil / Holm, Sverre / Rensen, Patrick C N / Dahl, Tuva B / Halvorsen, Bente

iScience

2024 Volume 27, Issue 4, Page(s) 109471

Abstract: Obesity is a complex multicausal disease that can cause morbidity and mortality, and there is need for improved knowledge on the underlying mechanisms. Using a mouse model of increased T cell responsiveness, we show that development of obesity can be ... ...

Abstract	Obesity is a complex multicausal disease that can cause morbidity and mortality, and there is need for improved knowledge on the underlying mechanisms. Using a mouse model of increased T cell responsiveness, we show that development of obesity can be driven by immune cells. This was confirmed with bone marrow transplantation and adoptive T cell transfer to several recipient mouse models. Single-cell RNA sequencing and CyTOF analysis showed that the mice display altered composition of circulating T cells and increased T cell activation in visceral adipose tissue, suggesting activated T cells as critical players in the increased fat mass. In this study, we provide evidence that obesity can be driven by immune cell activity and in particular by T cells, which could have broad implications for prevention and treatment of this condition.
Language	English
Publishing date	2024-03-11
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109471
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Article ; Online: Inhibition of the extracellular enzyme A disintegrin and metalloprotease with thrombospondin motif 4 prevents cardiac fibrosis and dysfunction.

Cardiovascular research

2023 Volume 119, Issue 10, Page(s) 1915–1927

Abstract: Aims: Heart failure is a condition with high mortality rates, and there is a lack of therapies that directly target maladaptive changes in the extracellular matrix (ECM), such as fibrosis. We investigated whether the ECM enzyme known as A disintegrin ... ...

Abstract	Aims: Heart failure is a condition with high mortality rates, and there is a lack of therapies that directly target maladaptive changes in the extracellular matrix (ECM), such as fibrosis. We investigated whether the ECM enzyme known as A disintegrin and metalloprotease with thrombospondin motif (ADAMTS) 4 might serve as a therapeutic target in treatment of heart failure and cardiac fibrosis. Methods and results: The effects of pharmacological ADAMTS4 inhibition on cardiac function and fibrosis were examined in rats exposed to cardiac pressure overload. Disease mechanisms affected by the treatment were identified based on changes in the myocardial transcriptome. Following aortic banding, rats receiving an ADAMTS inhibitor, with high inhibitory capacity for ADAMTS4, showed substantially better cardiac function than vehicle-treated rats, including ∼30% reduction in E/e' and left atrial diameter, indicating an improvement in diastolic function. ADAMTS inhibition also resulted in a marked reduction in myocardial collagen content and a down-regulation of transforming growth factor (TGF)-β target genes. The mechanism for the beneficial effects of ADAMTS inhibition was further studied in cultured human cardiac fibroblasts producing mature ECM. ADAMTS4 caused a 50% increase in the TGF-β levels in the medium. Simultaneously, ADAMTS4 elicited a not previously known cleavage of TGF-β-binding proteins, i.e. latent-binding protein of TGF-β and extra domain A-fibronectin. These effects were abolished by the ADAMTS inhibitor. In failing human hearts, we observed a marked increase in ADAMTS4 expression and cleavage activity. Conclusion: Inhibition of ADAMTS4 improves cardiac function and reduces collagen accumulation in rats with cardiac pressure overload, possibly through a not previously known cleavage of molecules that control TGF-β availability. Targeting ADAMTS4 may serve as a novel strategy in heart failure treatment, in particular, in heart failure with fibrosis and diastolic dysfunction.
MeSH term(s)	Rats ; Humans ; Animals ; Disintegrins/metabolism ; Disintegrins/pharmacology ; Myocardium/metabolism ; Heart Failure/metabolism ; Cardiomyopathies/metabolism ; Collagen/metabolism ; Fibroblasts/metabolism ; Transforming Growth Factor beta/metabolism ; Thrombospondins/metabolism ; Metalloproteases/metabolism ; Metalloproteases/pharmacology ; Fibrosis
Chemical Substances	Disintegrins ; Collagen (9007-34-5) ; Transforming Growth Factor beta ; Thrombospondins ; Metalloproteases (EC 3.4.-)
Language	English
Publishing date	2023-05-22
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvad078
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Article: Complement component C3 and the TLR co-receptor CD14 are not involved in angiotensin II induced cardiac remodelling

Shahini, Negar / Schjalm, Camilla / Nilsson, Per H / Holt, Margrethe Flesvig / Øgaard, Jonas D.S / Lien, Egil / Ahmed, Muhammad S / Attramadal, Håvard / Aukrust, Pål / Yndestad, Arne / Mollnes, Tom Eirik / Louwe, Mieke C

Biochemical and biophysical research communications. 2020 Mar. 19, v. 523, no. 4

2020

Abstract: Inflammation is centrally involved in the development of cardiac hypertrophy and the processes of remodelling. The complement system and Toll-like receptor (TLR) family, two upstream arms of the innate immune system, have previously been reported to be ... ...

Abstract	Inflammation is centrally involved in the development of cardiac hypertrophy and the processes of remodelling. The complement system and Toll-like receptor (TLR) family, two upstream arms of the innate immune system, have previously been reported to be involved in cardiac remodelling. However, the role of complement component 3 (C3), TLR co-receptor CD14 and the synergy between them have not been addressed during pressure overload-induced cardiac remodelling. Here, we examined angiotensin II-induced cardiac hypertrophy and remodelling for 7 days in male C57Bl/6 J mice deficient in C3, CD14, or both (C3CD14), and WT controls. Angiotensin II infusion induced a mild concentric hypertrophic phenotype in WT mice with increased left ventricle weight, wall thicknesses and reduced ventricular internal diameter, associated with increased cardiac fibrosis. However, there were no differences between WT mice and mice deficient for C3, CD14 or C3CD14, as systolic blood pressure, cardiac function and structure and levels of fibrosis were comparable between WT mice and the three other genotypes. C5a did not change in angiotensin II treated mice, whereas Mac2 levels were increased in angiotensin II treated mice, but did not differ between genotypes. The inflammatory IL-6 response was comparable between WT and C3 deficient mice, however, it was decreased in CD14 and C3CD14 deficient mice. We conclude that deficiency in C3, CD14 or C3CD14 had no effect on cardiac remodelling following angiotensin II-induced pressure overload. This suggests that C3 and CD14 are not involved in angiotensin II-induced adverse cardiac remodelling.
Keywords	Toll-like receptors ; cardiac output ; complement ; fibrosis ; hypertrophy ; inflammation ; innate immunity ; interleukin-6 ; males ; phenotype ; research ; systolic blood pressure
Language	English
Dates of publication	2020-0319
Size	p. 867-873.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.01.018
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Article ; Online: NLRP3 inflammasome mediates oxidative stress-induced pancreatic islet dysfunction.

Sokolova, Marina / Sahraoui, Afaf / Høyem, Merete / Øgaard, Jonas / Lien, Egil / Aukrust, Pål / Yndestad, Arne / Ranheim, Trine / Scholz, Hanne

American journal of physiology. Endocrinology and metabolism

2018 Volume 315, Issue 5, Page(s) E912–E923

Abstract: Inflammasomes are multiprotein inflammatory platforms that induce caspase-1 activation and subsequently interleukin (IL)-1β and IL-18 processing. The NLRP3 inflammasome is activated by different forms of oxidative stress, and, based on the central role ... ...

Abstract	Inflammasomes are multiprotein inflammatory platforms that induce caspase-1 activation and subsequently interleukin (IL)-1β and IL-18 processing. The NLRP3 inflammasome is activated by different forms of oxidative stress, and, based on the central role of IL-1β in the destruction of pancreatic islets, it could be related to the development of diabetes. We therefore investigated responses in wild-type C57Bl/6 (WT) mice, NLRP3
MeSH term(s)	Animals ; Apoptosis/physiology ; Diabetes Mellitus, Experimental/metabolism ; Inflammasomes/metabolism ; Insulin-Secreting Cells/metabolism ; Interleukin-1beta/metabolism ; Islets of Langerhans/metabolism ; Macrophage Activation/physiology ; Mice ; Mice, Knockout ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Oxidative Stress/physiology
Chemical Substances	Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2018-07-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603841-4
ISSN	1522-1555 ; 0193-1849
ISSN (online)	1522-1555
ISSN	0193-1849
DOI	10.1152/ajpendo.00461.2017
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