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Anti-CD8 treatment reduces the severity of inflammatory arthritis, but not vasculitis, in mercuric chloride-induced autoimmunity.

https://arctichealth.org/en/permalink/ahliterature14277
Source
Clin Exp Immunol. 1996 Nov;106(2):280-5
Publication Type
Article
Date
Nov-1996
Author
P D Kiely
D. O'Brien
D B Oliveira
Author Affiliation
Division of Renal Medicine, St George's Hospital Medical School, London, UK.
Source
Clin Exp Immunol. 1996 Nov;106(2):280-5
Date
Nov-1996
Language
English
Publication Type
Article
Keywords
Animals
Antibodies, Monoclonal - pharmacology
Antigens, CD8 - immunology
Arthritis - chemically induced - immunology - prevention & control
Autoantibodies - analysis
Autoimmunity - drug effects
CD8-Positive T-Lymphocytes - immunology
Cecal Diseases - chemically induced - immunology
Collagen - immunology
Enzyme-Linked Immunosorbent Assay
Immunoglobulin E - analysis
Interferon Type II - blood
Killer Cells, Natural - immunology
Lymphocyte Depletion
Lymphocyte Subsets - immunology
Mercuric Chloride - toxicity
Peroxidase - immunology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Vasculitis - chemically induced - immunology
Abstract
Mercuric chloride (HgCl2) induces a T cell-dependent autoimmune syndrome in Brown-Norway (BN) rats characterized by a humoral response, tissue injury with an accumulation of CD8+ and CD4+ T cells, and an increase in tissue IL-4 mRNA and serum IgE suggesting Th2 cell activation. In other models of autoimmune disease, CD8+ cells act in both anti- and pro-inflammatory capacities, suggesting that functionally distinct CD8+ populations exist in vivo. The effect of treatment with OX8, a depleting anti-CD8 MoAb, on the initiation of HgCl2-induced autoimmunity was assessed in two experiments in a total of 20 BN rats, and compared with 20 animals treated with a control MoAb or PBS. OX8 significantly depleted peripheral blood CD8+ lymphocytes, had no effect on HgCl2-induced anti-collagen or myeloperoxidase antibodies, nor on the incidence or severity of caecal vasculitis. The severity of HgCl2-induced arthritis was significantly reduced in OX8-treated animals; median peak score reduced from 7.5 to 3.0 (experiment 1) and from 7.0 to 4 (experiment 2) (P = 0.009, Mann-Whitney U-test). OX8 treatment also exacerbated the early rise in HgCl2-induced IgE and induced a significant rise in plasma interferon-gamma (IFN-gamma), suggesting that CD8+ cells may have a regulatory influence on Th cell populations. These data provide direct evidence that CD8+ cells may act in a proinflammatory capacity in both this model of autoimmunity and the pathogenesis of inflammatory arthritis.
PubMed ID
8918574 View in PubMed
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Association between the use of serotonin receptor 2A-blocking antidepressants and joint disorders.

https://arctichealth.org/en/permalink/ahliterature95083
Source
Arthritis Rheum. 2009 Oct 15;61(10):1322-7
Publication Type
Article
Date
Oct-15-2009
Author
Kling Anders
Danell-Boman Marit
Stenlund Hans
Dahlqvist Rune
Author Affiliation
University Hospital, Umeå, Sweden. anders.kling@pharm.umu.se
Source
Arthritis Rheum. 2009 Oct 15;61(10):1322-7
Date
Oct-15-2009
Language
English
Publication Type
Article
Keywords
Adverse Drug Reaction Reporting Systems
Aged
Arthralgia - chemically induced - epidemiology
Arthritis - chemically induced - epidemiology
Databases, Factual
Female
Humans
Male
Middle Aged
Receptor, Serotonin, 5-HT2A - antagonists & inhibitors
Retrospective Studies
Serotonin Uptake Inhibitors - adverse effects
Sweden - epidemiology
Abstract
OBJECTIVE: There are case reports about antidepressants causing arthritis and arthralgia, and the majority of these reports deal with atypical antidepressants, which are serotonin receptor 2A (5-HT(2A))-blocking substances. The aim of this study was to examine a possible association between joint disorders and the use of 5-HT(2A)-blocking atypical antidepressants. METHODS: We performed a retrospective study using reports of adverse drug reactions (ADRs) of 5-HT(2A)-blocking atypical antidepressant substances concerning joint disorders reported to the Swedish Adverse Drug Reactions Committee and the World Health Organization (WHO) Adverse Reactions Database during the period January 1, 1990 to December 31, 2006. The reports of joint disorders were related to sales figures measured as defined daily doses and to the total number of ADR reports. RESULTS: In the Swedish material, the 5-HT(2A) antagonists were 45 times more often reported to give joint ADRs when related to sales figures and compared with the selective serotonin reuptake inhibitors (SSRIs; P
PubMed ID
19790123 View in PubMed
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[Formaldehyde in textiles as a possible cause of arthritis and angioedema]

https://arctichealth.org/en/permalink/ahliterature14446
Source
Ugeskr Laeger. 1992 Jan 13;154(3):141-2
Publication Type
Article
Date
Jan-13-1992
Author
O C Jensen
B. Bach
Author Affiliation
Arbejdsmedicinsk afdeling, Skive Sygehus.
Source
Ugeskr Laeger. 1992 Jan 13;154(3):141-2
Date
Jan-13-1992
Language
Danish
Publication Type
Article
Keywords
Adult
Angioneurotic Edema - chemically induced
Arthritis - chemically induced
Denmark
English Abstract
Female
Formaldehyde - adverse effects
Humans
Occupational Diseases - chemically induced
Textile Industry
Abstract
A case of arthritis and angioedema which developed on occupational exposure to formaldehyde in textiles is described. Possible pathological mechanisms are discussed. The suspicion that an unknown immunological reaction may be the cause is raised.
PubMed ID
1738955 View in PubMed
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Inflammatory polyarthritis induced by mercuric chloride in the Brown Norway rat.

https://arctichealth.org/en/permalink/ahliterature14329
Source
Lab Invest. 1995 Aug;73(2):284-93
Publication Type
Article
Date
Aug-1995
Author
P D Kiely
S. Thiru
D B Oliveira
Author Affiliation
Department of Medicine, University of Cambridge School of Clinical Medicine, Addenbrooke's Hospital, United Kingdom.
Source
Lab Invest. 1995 Aug;73(2):284-93
Date
Aug-1995
Language
English
Publication Type
Article
Keywords
Animals
Antibodies, Monoclonal - immunology
Arthritis - chemically induced - immunology
Collagen - immunology
Female
Male
Mercuric Chloride - toxicity
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
T-Lymphocytes, Helper-Inducer - immunology
Abstract
BACKGROUND: Mercuric chloride (HgCl2) induces an autoimmune syndrome in susceptible strains of rodent. In the Brown Norway (BN) rat, this is characterized by autoreactive T cells, high levels of total IgE, IgG autoantibodies, including anti-collagen types I and II, and tissue injury, including glomerulonephropathy and necrotizing vasculitis of the gut. The high total IgE levels and evidence showing ex vivo down-regulation of IFN gamma and in vivo up-regulation of IL-4 suggest that HgCl2-induced autoimmunity occurs in a Th2 lymphokine environment. EXPERIMENTAL DESIGN: HgCl2-autoimmunity was induced in BN rats using standard methods. Anti-collagen (types I and II) Ab and IgG subclasses were measured by ELISA. Arthritis was scored on Days 13 to 17 after HgCl2 treatment. Ankle joints and synovium were examined with standard histologic and immunohistochemical techniques. The incidence and severity of arthritis were compared in normal and R73 (anti-alpha/beta T cell receptor mAb)-treated BN rats. After R73 treatment, T cell function was assessed by measuring the total IgE and anti-type II collagen response to HgCl2, and FACS was used to assess the number of peripheral blood OX19+ lymphocytes (T cell marker). RESULTS: A self-limiting inflammatory arthritis develops in more than 82% of animals and is more severe in males. Histologically, there is a predominant ED1+ macrophage synovial infiltrate, areas of fibrinoid necrosis, and vasculitis and erosions of cartilage. The peak anti-collagen (type I and II) Ab titer does not correlate with arthritis incidence or severity. Treatment with R73 markedly reduces the rise in total IgE and IgG anti-type II collagen, reduces OX19+ peripheral blood lymphocytes, and abolishes the arthritis. CONCLUSIONS: HgCl2 induces a T cell-dependent inflammatory arthritis in the BN rat. In contrast with other animal models, HgCl2-induced arthritis is associated with an apparent Th2 lymphokine response.
PubMed ID
7637329 View in PubMed
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Oxpentifylline inhibits tumor necrosis factor-alpha mRNA transcription and protects against arthritis in mercuric chloride-treated brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature14326
Source
Eur J Immunol. 1995 Oct;25(10):2899-906
Publication Type
Article
Date
Oct-1995
Author
P D Kiely
K M Gillespie
D B Oliveira
Author Affiliation
Department of Medicine, University of Cambridge School of Clinical Medicine, GB.
Source
Eur J Immunol. 1995 Oct;25(10):2899-906
Date
Oct-1995
Language
English
Publication Type
Article
Keywords
Animals
Arthritis - chemically induced - immunology - pathology - prevention & control
Autoimmune Diseases - chemically induced - immunology - pathology - prevention & control
Cecal Diseases - chemically induced - immunology - pathology - prevention & control
Disease Models, Animal
Humans
Immunoglobulin E - biosynthesis - genetics
Interleukin-4 - biosynthesis - genetics
Mercuric Chloride - toxicity
Pentoxifylline - pharmacology - therapeutic use
RNA, Messenger - biosynthesis - genetics
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Tumor Necrosis Factor-alpha - biosynthesis - genetics
Vasculitis - chemically induced - immunology - pathology - prevention & control
Abstract
The phosphodiesterase inhibitor oxpentifylline (OXP) has a number of potentially important immunomodulatory actions which include a selective inhibition of the Th1 subset of CD4+ cells in vitro and inhibition of tumor necrosis factor (TNF)-alpha mRNA transcription. In vivo, it has a dramatic protective effect against experimental allergic encephalomyelitis. In this animal model, tissue injury is associated with both a Th1 response and with TNF-alpha production, either of which could be targets for the protective action of OXP. In an attempt to clarify the relative importance of the Th cell subsets and TNF-alpha in pathogenesis, we investigated the effect of OXP on a Th2 model of T cell-dependent disease, mercuric chloride (HgCl2)-induced autoimmunity in the Brown Norway rat. The effects of OXP on the Th1:Th2 response, TNF-alpha mRNA transcription in spleen and ankle joints, and on the incidence and severity of arthritis and cecal vasculitis have been examined and the effects in vivo have been compared with those of a soluble TNF receptor-IgG1 fusion protein (sTNFR) that neutralizes rat TNF-alpha. In two separate experiments, OXP significantly enhanced unstimulated levels of splenic interleukin-4 (IL-4) mRNA (median 62%, of an artificial IL-4 mRNA construct, vs. 36.5% in controls) and in one experiment, exaggerated the total IgE response to HgCl2. OXP inhibited HgCl2-induced TNF-alpha mRNA transcription in spleen and ankle joints. In three separate experiments, OXP had a significant protective effect against arthritis, with the mean incidence reduced from 100% to 30% and mean peak score reduced from 7.2 to 2.59 (experiments 1 and 2). The protection against arthritis was indistinguishable from that produced by sTNFR. There was no such protection against cecal vasculitis with either OXP or sTNFR. These results demonstrate that OXP induces a shift towards a Th2 response, inhibits TNF-alpha mRNA transcription locally in joint and systemically in spleen, and has a protective effect against arthritis similar to that produced by sTNFR in the HgCl2-treated BN rat. We conclude that TNF-alpha is a critical cytokine in the pathogenesis of arthritis but not cecal vasculitis in this model, and that inhibition of TNF-alpha transcription is the most important mode of action of OXP in this situation. OXP may be a potential therapeutic agent in the treatment of other arthritides, such as human rheumatoid arthritis, in which TNF-alpha has been implicated in pathogenesis.
PubMed ID
7589090 View in PubMed
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6 records – page 1 of 1.