31 results match your criteria pristane loss


Loss of microRNA-147 function alleviates synovial inflammation through ZNF148 in rheumatoid and experimental arthritis.

Eur J Immunol 2021 Apr 17. Epub 2021 Apr 17.

Department of Biochemistry and Molecular Biology, Institute of Molecular and Translational Medicine (IMTM), School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, P. R. China.

MicroRNA-147 (miR-147) had been previously found induced in synoviocytes by inflammatory stimuli derived from T cells in experimental arthritis. This study was designed to verify whether loss of its function might alleviate inflammatory events in joints of experimental and rheumatoid arthritis (RA). Dark Agouti (DA) rats were injected intradermally with pristane to induce arthritis, and rno-miR-147 antagomir was locally administrated into individual ankle compared with negative control or rno-miR-155-5p antagomir (potential positive control). Read More

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Hypertension and endothelial dysfunction in the pristane model of systemic lupus erythematosus.

Physiol Rep 2021 Feb;9(3):e14734

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA.

Autoimmune diseases such as psoriasis, rheumatoid arthritis, and systemic lupus erythematosus (SLE) have high rates of hypertension and cardiovascular disease. Systemic lupus erythematosus is a prototypic autoimmune disorder that primarily affects women of childbearing age and is associated with a loss of self-tolerance, autoreactive B and T lymphocytes, and the production of autoantibodies, especially to nuclear components. In this study, we hypothesized that the pristane-inducible model of SLE would develop hypertension and vascular dysfunction as the disease progressed. Read More

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February 2021

The peptide symporter SLC15a4 is essential for the development of systemic lupus erythematosus in murine models.

PLoS One 2021 14;16(1):e0244439. Epub 2021 Jan 14.

DiCE Molecules, South San Francisco, CA, United States of America.

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disease representing a serious unmet medical need. The disease is associated with the loss of self-tolerance and exaggerated B cell activation, resulting in autoantibody production and the formation of immune complexes that accumulate in the kidney, causing glomerulonephritis. TLR7, an important mediator of the innate immune response, drives the expression of type-1 interferon (IFN), which leads to expression of type-1 IFN induced genes and aggravates lupus pathology. Read More

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Oxidative DNA Damage Accelerates Skin Inflammation in Pristane-Induced Lupus Model.

Front Immunol 2020 24;11:554725. Epub 2020 Sep 24.

Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, CA, United States.

Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disease in which type I interferons (IFN) play a key role. The IFN response can be triggered when oxidized DNA engages the cytosolic DNA sensing platform cGAS-STING, but the repair mechanisms that modulate this process and govern disease progression are unclear. To gain insight into this biology, we interrogated the role of oxyguanine glycosylase 1 (OGG1), which repairs oxidized guanine 8-Oxo-2'-deoxyguanosine (8-OH-dG), in the pristane-induced mouse model of SLE. Read More

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Syk inhibitor attenuates inflammation in lupus mice from FcgRIIb deficiency but not in pristane induction: the influence of lupus pathogenesis on the therapeutic effect.

Lupus 2020 Sep 22;29(10):1248-1262. Epub 2020 Jul 22.

Department of Microbiology, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.

Macrophages are responsible for the recognition of pathogen molecules. The downstream signalling of the innate immune responses against pathogen molecules, lipopolysaccharide (LPS) and (1→3)-β-D-glucan (BG), and the adaptive immune response to antibodies, Fc gamma receptor (FcgR), is spleen tyrosine kinase (Syk). Because pathogen molecules and antibodies could be presented in lupus, impact of Syk and macrophages in lupus is explored. Read More

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September 2020

CD4CD69 T cells and CD4CD25FoxP3 Treg cells imbalance in peripheral blood, spleen and peritoneal lavage from pristane-induced systemic lupus erythematosus (SLE) mice.

Adv Rheumatol 2019 07 24;59(1):30. Epub 2019 Jul 24.

Laboratório de Imunologia Celular (LIM-17) - Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de Sao Paulo, Sao Paulo, SP, Brazil.

Background: Adaptive immune cells, including CD4CD69 and CD4CD25FoxP3 regulatory T (Treg) cells, are important for maintaining immunological tolerance. In human systemic lupus erythematosus (SLE), CD4CD25FoxP3 Treg cells are reduced, whereas CD69 expression is increased, resulting in a homeostatic immune imbalance that may intensify autoreactive T cell activity. To analyze the mechanisms implicated in autotolerance failure, we evaluated CD4CD69 and CD4CD25FoxP3 T cells and interleukin profiles in a pristane-induced SLE experimental model. Read More

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WDFY4 Is Involved in Symptoms of Systemic Lupus Erythematosus by Modulating B Cell Fate via Noncanonical Autophagy.

J Immunol 2018 11 26;201(9):2570-2578. Epub 2018 Sep 26.

Key Laboratory for Experimental Teratology of the Ministry of Education, Shandong University School of Medicine, Jinan, Shandong 250012, China;

Genome-wide association studies have recently illuminated that is genetically associated with systemic lupus erythematosus (SLE) susceptibility in various ethnic groups. Despite strong genetic evidence suggesting a role of in SLE pathogenesis, its functional relevance is largely unknown. In this study, we generated B lymphocyte conditional knockout (-CKO) mice and found that loss of led to a decrease in number of total B cells and several subpopulations of B cells in the periphery and a defect in the transition from the pro- to pre-B cell stage in bone marrow. Read More

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November 2018

IL-17C/IL-17 Receptor E Signaling in CD4 T Cells Promotes T17 Cell-Driven Glomerular Inflammation.

J Am Soc Nephrol 2018 04 26;29(4):1210-1222. Epub 2018 Feb 26.

III. Medizinische Klinik, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany

The IL-17 cytokine family and the cognate receptors thereof have a unique role in organ-specific autoimmunity. Most studies have focused on the founding member of the IL-17 family, IL-17A, as the central mediator of diseases. Indeed, although pathogenic functions have been ascribed to IL-17A and IL-17F in the context of immune-mediated glomerular diseases, the specific functions of the other IL-17 family members in immunity and inflammatory kidney diseases is largely unknown. Read More

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Regulation of Leukocyte Recruitment to the Spleen and Peritoneal Cavity during Pristane-Induced Inflammation.

J Immunol Res 2017 19;2017:9891348. Epub 2017 Oct 19.

Department of Basic Medicine, Haihe Clinical College of Tianjin Medical University, Tianjin, China.

Chronic inflammation is associated with an increased number of leukocytes in the spleen, which are then redirected to the site of inflammation. However, it remains unknown how leukocyte recruitment is regulated. Herein, chronic inflammation was induced by intraperitoneal injection of pristane into mice. Read More

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Development of pristane induced mice model for lupus with atherosclerosis and analysis of TLR expression.

Clin Exp Rheumatol 2016 Jul-Aug;34(4):600-8. Epub 2016 Jun 22.

Department of Rheumatology and Immunology, the Second Affiliated Hospital of Fujian Medical University, Quanzhou, China.

Objectives: This study was designed to establish a murine model of lupus with atherosclerosis, and to investigate the expression of Toll-like receptors (TLRs) in the aorta and kidney.

Methods: The 9-week-old female ApoE-/- and C57BL/6 mice were randomly divided into a ApoE-/- pristane treated group (group A), ApoE-/- control group (group B), C57BL/6 pristane treated group (group C) and C57BL/6 control group (group D). Each mouse was given either a single intraperitoneal injection of 0. Read More

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September 2016

Animal Models of Rheumatoid Arthritis (I): Pristane-Induced Arthritis in the Rat.

PLoS One 2016 26;11(5):e0155936. Epub 2016 May 26.

Division of Medical Inflammation Research, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.

Background: To facilitate the development of therapies for rheumatoid arthritis (RA), the Innovative Medicines Initiative BTCure has combined the experience from several laboratories worldwide to establish a series of protocols for different animal models of arthritis that reflect the pathogenesis of RA. Here, we describe chronic pristane-induced arthritis (PIA) model in DA rats, and provide detailed instructions to set up and evaluate the model and for reporting data.

Methods: We optimized dose of pristane and immunization procedures and determined the effect of age, gender, and housing conditions. Read More

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Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus.

J Immunol 2013 Sep 5;191(5):2104-14. Epub 2013 Aug 5.

Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Loss-of-function mutations in the Fas death receptor or its ligand result in a lymphoproliferative syndrome and exacerbate clinical disease in most lupus-prone strains of mice. One exception is mice injected with 2,6,10,14-tetramethylpentadecane (TMPD), a hydrocarbon oil commonly known as pristane, which induces systemic lupus erythematosus-like disease. Although Fas/Fas ligand (FasL) interactions have been strongly implicated in the activation-induced cell death of both lymphocytes and other APCs, FasL can also trigger the production of proinflammatory cytokines. Read More

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September 2013

Monocytes from Irf5-/- mice have an intrinsic defect in their response to pristane-induced lupus.

J Immunol 2012 Oct 29;189(7):3741-50. Epub 2012 Aug 29.

Department of Biochemistry and Molecular Biology, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.

The transcription factor IFN regulatory factor (IRF)5 has been identified as a human systemic lupus erythematosus (SLE) susceptibility gene by numerous joint linkage and genome-wide association studies. Although IRF5 expression is significantly elevated in primary blood cells of SLE patients, it is not yet known how IRF5 contributes to SLE pathogenesis. Recent data from mouse models of lupus indicate a critical role for IRF5 in the production of pathogenic autoantibodies and the expression of Th2 cytokines and type I IFN. Read More

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October 2012

Irf5-deficient mice are protected from pristane-induced lupus via increased Th2 cytokines and altered IgG class switching.

Eur J Immunol 2012 Jun;42(6):1477-87

Department of Biochemistry & Molecular Biology, New Jersey Medical School, UMDNJ, Newark, NJ 07103, USA.

Polymorphisms in the transcription factor interferon (IFN) regulatory factor 5 (IRF5) have been identified that show a strong association with an increased risk of developing the autoimmune disease systemic lupus erythematosus (SLE). A potential pathological role for IRF5 in SLE development is supported by the fact that increased IRF5 mRNA and protein are observed in primary blood cells of SLE patients and this correlates with an increased risk of developing the disease. Here, we demonstrate that IRF5 is required for pristane-induced SLE via its ability to control multiple facets of autoimmunity. Read More

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Periodontitis and arthritis interaction in mice involves a shared hyper-inflammatory genotype and functional immunological interferences.

Genes Immun 2010 Sep 29;11(6):479-89. Epub 2010 Apr 29.

Department of Biochemistry and Immunology, School of Medicine of Ribeirão Preto--FMRP/USP, Sao Paulo, Brazil.

Periodontitis (PD) and rheumatoid arthritis (RA) have been found to be clinically associated and to share the chronic nature of the inflammatory reaction associated with bone resorption activity. However, the mechanisms underlying such association are unknown. Therefore, we examined the basis of Actinobacillus actinomycetemcomitans- and Porphyromonas gingivalis-induced PD and pristane-induced arthritis (PIA) interaction in mice. Read More

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September 2010

Profound and paradoxical impact on arthritis and autoimmunity of the rat antigen-presenting lectin-like receptor complex.

Arthritis Rheum 2008 May;58(5):1343-53

Center for Molecular Medicine, Stockholm, Sweden.

Objective: The antigen-presenting lectin-like receptor complex (APLEC) was recently identified as a genetic determinant for arthritis susceptibility. We undertook this study to define mechanisms underlying the impact of APLEC on arthritis, to determine whether sex effects occur, and to determine whether APLEC influences different types of arthritis and phenotypes other than susceptibility.

Methods: Arthritis-susceptible DA rats were compared with sex-matched congenic rats in which APLEC alleles were substituted with alleles from arthritis-resistant PVG rats. Read More

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Utility of lipid biomarkers in support of bioremediation efforts at army sites.

J Microbiol Methods 2008 Jul 21;74(1):17-25. Epub 2007 Jul 21.

U.S. Army ERDC-CRREL, 72 Lyme Rd., Hanover, NH 03755, United States.

Lipid biomarker analysis has proven valuable in testing the hypothesis that attributes of the extant microbiota can directly reflect the occurrence of contaminant biodegradation. Two past research efforts have demonstrated this utility and are described here. A 4. Read More

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Petroleum pollutant degradation by surface water microorganisms.

Environ Sci Pollut Res Int 2006 Sep;13(5):320-7

Center of Chemistry, IChTM, Belgrade, Serbia & Montenegro.

Background, Aims And Scope: It is well known that the composition of petroleum or some of its processing products changes in the environment mostly under the influence of microorganisms. A series of experiments was conducted in order to define the optimum conditions for an efficient biodegradation of petroleum pollutant, or bioremediation of different segments of the environment. The aim of these investigations was to show to what extent the hydrocarbons of a petroleum pollutant are degraded by microbial cultures which were isolated as dominant microorganisms from a surface water of a wastewater canal of an oil refinery and a nitrogen plant. Read More

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September 2006

Hypercatabolism of IgG in mice with lupus-like syndrome.

Lupus 2005 ;14(6):458-66

Cancer Immunobiology Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.

The metabolism of radioiodinated mouse IgG was studied in mice with lupus-like syndrome before and after the onset of the disease. Before the onset of the disease, the pharmacokinetic parameters of IgG in MLR-1pr and Pristane-primed Balb/c mice were within the normal range of values. After the onset of the disease a considerable increase in the catabolic rate of IgG was recorded abbreviating its half life to less than one third of the normal value. Read More

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November 2005

Application of a slow-release fertilizer for oil bioremediation in beach sediment.

J Environ Qual 2004 Jul-Aug;33(4):1210-6

Department of Chemical and Biomolecular Engineering, 4 Engineering Drive 4, National University of Singapore, Singapore 117576.

A 105-d field experiment was conducted to determine the potential of the slow-release fertilizer, Osmocote (Scotts, Marysville, OH), to stimulate the indigenous microbial biodegradation of petroleum hydrocarbons in an oil-spiked beach sediment on an intertidal foreshore in Singapore. Triplicate microcosms containing 80 kg of weathered sediment, spiked with 5% (w/w) Arabian light crude oil and 1.2% (w/w) Osmocote pellets, were established, together with control microcosms minus Osmocote. Read More

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January 2005

Effect of nutrient amendments on indigenous hydrocarbon biodegradation in oil-contaminated beach sediments.

J Environ Qual 2003 Jul-Aug;32(4):1234-43

Department of Chemical and Environmental Engineering, National University of Singapore, 10 Kent Ridge Crescent, Singapore 119260.

Nutrient amendment to oil-contaminated beach sediments is a critical factor for the enhancement of indigenous microbial activity and biodegradation of petroleum hydrocarbons in the intertidal marine environment. In this study, we investigated the stimulatory effect of the slow-release fertilizers Osmocote (Os; Scotts, Marysville, OH) and Inipol EAP-22 (Ip; ATOFINA Chemicals, Philadelphia, PA) combined with inorganic nutrients on the bioremediation of oil-spiked beach sediments using an open irrigation system with artificial seawater over a 45-d period. Osmocote is comprised of a semipermeable membrane surrounding water-soluble inorganic N, P, and K. Read More

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November 2003

The impact of p53 loss on murine plasmacytoma development.

Chromosome Res 2002 ;10(3):239-51

Manitoba Institute of Cell Biology, The Genomic Centre for Cancer Research and Diagnosis, Department of Physiology, The University of Manitoba, Winnipeg, Canada.

Mouse plasmacytomas (PCTs) are characterized by c-myc-activating translocations that juxtapose c-myc on chromosome 15 onto one of the immunoglobulin loci (IgH on chromosome 12, IgK on chromosome 6, or IgA on chromosome 16). To assess the impact of p53 loss on PCT genesis, we induced PCTs in p53-deficient BALB/cRb6.15 mouse strains. Read More

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December 2002

Allele-specific loss or imbalance of chromosomes 9, 15, and 16 in B-cell tumors from interspecific F1 hybrid mice carrying Emu-c-myc or N-myc transgenes.

Int J Cancer 2000 Dec;88(6):920-7

Beatson Institute for Cancer Research, Department of Medical Oncology, University of Glasgow, Glasgow, United Kingdom.

Mice carrying an immunoglobulin enhancer (Emu-) linked c- or N-myc transgene develop fatal monoclonal or oligoclonal pre-B or B-cell lymphomas. This indicates that, beside the Emu-activated myc gene, additional genetic changes are required for tumor development. To trace these additional changes, we carried out a genome-wide search for loss of heterozygosity (LOH) and allelic imbalance (AI). Read More

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December 2000

Germline CDKN2A mutation implicated in predisposition to multiple myeloma.

Blood 2000 Mar;95(5):1869-71

Departments of Medical Biophysics, Clinical Science, and Medicine, University of Toronto, Toronto, Ontario, Canada.

Germline mutations of the CDKN2A (p16(INK4A)) tumor suppressor gene predispose patients to melanoma and pancreatic carcinoma. In contrast, mutations of the murine CDKN2A gene predispose BALB/c mice to pristane-induced plasmacytoma. We describe here a family in which a germline mutation of CDKN2A is present in 4 individuals who developed melanoma as well as in a fifth family member who is suffering from multiple myeloma. Read More

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The fate of heavy oil wastes in soil microcosms. I: A performance assessment of biotransformation indices.

Sci Total Environ 1999 Feb;226(1):1-22

National Centre for Risk Analysis and Options Appraisal, Environment Agency, London, UK.

A controlled soil microcosm study was used to evaluate the performance of selected oil biotransformation indices using samples of Nigerian crude, a blended ballast oil and No. 6 fuel oil. Biotic losses were demonstrated through loss of solvent extractable matter (SEM) and changes in class fraction distribution in weathered soil extracts relative to sterilised controls. Read More

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February 1999

Perturbation of B cell genesis in the bone marrow of pristane-treated mice. Implications for plasmacytoma induction.

J Immunol 1995 Mar;154(5):2082-91

Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada.

A single injection of pristane was given i.p. to plasmacytoma-susceptible BALB/cAn mice. Read More

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Differences in the molecular structure of c-myc-activating recombinations in murine plasmacytomas and precursor cells.

Proc Natl Acad Sci U S A 1994 Dec;91(25):12066-70

Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.

The translocation of c-myc on chromosome (chr.) 15 to an immunoglobulin heavy-chain switch region on chr. 12 is the critical oncogenic step in pristane-induced plasmacytoma (PCT) development in BALB/cAnPt mice. Read More

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December 1994

Induction of plasmacytomas with silicone gel in genetically susceptible strains of mice.

J Natl Cancer Inst 1994 Jul;86(14):1058-65

Division of Cancer Biology, National Cancer Institute, Bethesda, Md 20892.

Background: Plasmacytomas can be induced in high frequency in susceptible strains of mice by the intraperitoneal introduction of plastics or paraffin oils, including the chemically defined oil pristane (2,6,10,14-tetramethylpentadecane). These materials persist in the peritoneal cavity, where they induce chronic inflammation during the long periods before plasmacytomas develop. Such plasmacytomas appear to arise from B cells carrying chromosomal translocations that affect c-myc transcription. Read More

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Mediators of joint swelling and damage in rheumatoid arthritis and pristane induced arthritis.

Autoimmunity 1992 ;13(4):327-31

Department of Pathology, School of Medical Sciences, University of Bristol, UK.

Joint swelling and tenderness in rheumatoid arthritis (RA) probably result from IgG aggregates activating complement with the consequent attraction of polymorphonuclear leucocytes (PMNs) and the liberation of their granule enzymes such as kininogenases. By contrast IL-1 and TNF are the major stimulants of cartilage and bone loss although other agents contribute. The fundamental drive for the production of these mediators is unknown but a role for heat shock proteins is suggested from work on pristane induced arthritis. Read More

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February 1993

Proliferation of B cell precursors in bone marrow of pristane-conditioned and malaria-infected mice: implications for B cell oncogenesis.

Curr Top Microbiol Immunol 1990 ;166:149-57

Department of Anatomy, McGill University, Montreal, Quebec, Canada.

Two widely different agents implicated in the etiology of neoplasias of the B cell lineage, pristane and malaria, have both been found to produce a prolonged increase in the level of proliferative activity and cell production by early B lymphocyte precursor cells in mouse bone marrow. This apparently leads to an elevated level of cell loss, suggesting the production of many aberrant early cells. The mechanism and significance of this effect remain to be determined. Read More

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