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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The maedi-visna virus (MVV) is classified as a lentivirus of the retroviridae family. The genome of MVV includes three genes: gag, which encodes for group-specific antigens; pol, which encodes for reverse transcriptase, integrase, RNAse H, protease and dUTPase and env, the gene encoding for the surface glycoprotein responsible for receptor binding and entry of the virus into its host cell. In addition, analogous to other lentiviruses, the genome contains genes for regulatory proteins, i.e. vif, rev and tat. The coding regions of the genome are flanked by long terminal repeats (LTR) which play a crucial role in the replication of the viral genome and provide binding sites for cellular transcription factors. The organs targeted by MVV are, in descending order of importance, the lungs, mammary glands, joints and the brain. In these organs, the virus replicates in mature macrophages and induces slowly progressing inflammatory lesions containing B and T lymphocytes. The clinical signs of MVV infection, i.e. dyspnea, loss of weight, mastitis and arthritis, are related to the location of these lesions. Infection with MVV induces the formation of antibodies which can be detected by agar gel immunodiffusion, ELISA and the serum neutralization assay. As neither antiviral treatment nor vaccination is available, diagnostic tests are the backbone of most of the schemes implemented to prevent the spread of MVV. However, since current serological assays are still lacking in sensitivity and specificity, molecular biological methods are being developed permitting the detection of virus in peripheral blood, milk and tissue samples. Future research will have to focus on both the development of new diagnostic tests and a better understanding of the pathogenesis of MVV infection.
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PMID:Maedi-visna virus infection in sheep: a review. 968 46

Infection of susceptible mouse strains with Borrelia burgdorferi, the agent of Lyme disease, results in the development of arthritis. Components of the innate immune system may be important mediators of this pathology. To investigate the potential role of NK cells in development of experimental Lyme arthritis, we examined their activation in vivo in both resistant and susceptible mouse strains. Following inoculation of B. burgdorferi into the footpad, lymph node NK cells from susceptible C3H/HeJ (C3H) mice produced more gamma interferon than NK cells from resistant DBA/2J mice. Lymph node cells from susceptible C3H and AKR mice also had increased ability to lyse YAC-1 target cells 2 days following infection. Antibody depletion of NK cells from susceptible mice, however, did not alter the development of arthritis following B. burgdorferi challenge. In addition, NK cell depletion had little effect on spirochete burden. Thus, there is a marked activation of NK cells in susceptible mouse strains following infection. Although NK cells are not absolutely required for arthritis, events occurring prior to NK cell activation might be important in mediating pathology in experimental Lyme disease.
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PMID:Activation of natural killer cells in arthritis-susceptible but not arthritis-resistant mouse strains following Borrelia burgdorferi infection. 978 24

The specificity of infection-induced immunity in mice infected with cultured or host-adapted Borrelia burgdorferi sensu lato, the agent of Lyme disease, was examined. Sera obtained from mice following infection with high and low doses of cultured B. burgdorferi sensu stricto, transplantation of infected tissue (host-adapted spirochetes), or tick-borne inoculation all showed protective activity in passive immunization assays. Infection and disease were similar in mice infected with cultured spirochetes or by transplantation. Thus, the adaptive form of inoculated spirochetes did not influence the immune response during active infection. Mice infected with B. burgdorferi sensu stricto and then cured of infection with an antibiotic during early or late stages of infection were resistant to challenge with high doses of homologous cultured spirochetes for up to 1 year. In contrast, actively immune mice infected with different Borrelia species (B. burgdorferi sensu lato, B. burgdorferi sensu stricto cN40, Borrelia afzelii PKo, and Borrelia garinii PBi) and then treated with an antibiotic were resistant to challenge with cultured homologous but not heterologous spirochetes. Similar results were achieved for actively immune mice challenged by transplantation and by passive immunization with sera from mice infected with each of the Borrelia species and then challenged with cultured spirochetes. Arthritis and carditis in mice that had immunizing infections with B. afzelii and B. garinii and then challenged by transplantation with B. burgdorferi sensu stricto were equivalent in prevalence and severity to those in nonimmune recipient mice. These results indicate that protective immunity and disease-modulating immunity that develop during active infection are universal among species related to B. burgdorferi sensu lato but are species specific.
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PMID:Specificity of infection-induced immunity among Borrelia burgdorferi sensu lato species. 986 93

Synovial fibroblasts probably represent host cells for Chlamydia trachomatis during initial intra-articular infection in reactive arthritis. In vitro synovial cells produce interferon-beta (IFN-beta) in response to chlamydial infection. IFN-beta expression can be activated by interferon regulatory factor-1 (IRF-1) and interferon-stimulated gene factor 3gamma (ISGF3gamma). In this study, we demonstrate that infection of synovial fibroblasts with C. trachomatis serotype D induced the expression of IRF-1 mRNA as shown by reverse transcription-PCR. Tumor necrosis factor-alpha (TNF-alpha) stimulation enhanced IRF-1 mRNA levels in infected cells and was required to detect IRF-1 protein by immunoblotting. The level of constitutively expressed IRF-2 was not significantly affected after infection. C. trachomatis was found to cause an up-regulation of ISGF3gamma protein in synovial cells. Induction of the tryptophan-catabolizing enzyme indoleamine 2,3-dioxygenase (IDO) is an important mechanism of the host cell response to control intracellular infection by chlamydiae. It has been described that IRF-1 can induce IDO gene expression. Infection of synovial fibroblasts alone in the absence of exogenous cytokine induced the expression of IDO mRNA which was enhanced by TNF-alpha treatment. The stimulation of IRF-1, ISGF3gamma, and IDO expression was most effective when viable chlamydiae were used as inoculum. Neutralization of IFN-beta in the culture medium of infected cells diminished but did not abrogate expression of IRF-1, ISGF3gamma, and IDO. The increased production of IRF-1 and ISGF3gamma in C. trachomatis-infected synovial fibroblasts may contribute to induction of IFN-beta and IDO.
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PMID:Expression of interferon regulatory factors and indoleamine 2,3-dioxygenase in Chlamydia trachomatis-infected synovial fibroblasts. 1036 77

Yersinia-induced reactive arthritis is highly associated with HLA-B27, the role of which in defense against the triggering bacteria remains unclear. The aim of this study was to examine the capacity of rats transgenic for HLA-B27 to mount a cytotoxic T-lymphocyte (CTL) response against Y. pseudotuberculosis and to determine the influence of the HLA-B27 transgene on this response. Rats transgenic for HLA-B*2705 and human beta(2)-microglobulin of the 21-4L line, which do not spontaneously develop disease, and nontransgenic syngeneic Lewis (LEW) rats were infected with Y. pseudotuberculosis. Lymph node cells were restimulated in vitro, and the presence of for Y. pseudotuberculosis-specific CTLs against infected targets was determined. Infection of 21-4L rats triggered a CD8(+) T cell-mediated cytotoxic response specific for Y. pseudotuberculosis. Analysis of this response demonstrated restriction by an endogenous major histocompatibility complex molecule. However, no restriction by HLA-B27 was detected. In addition, kinetics studies revealed a weaker anti-Yersinia CTL response in 21-4L rats than in nontransgenic LEW rats, and the level of cytotoxicity against 21-4L lymphoblast targets sensitized with Y. pseudotuberculosis was lower than that against nontransgenic LEW targets. We conclude that HLA-B27 transgenic rats mount a CTL response against Y. pseudotuberculosis that is not restricted by HLA-B27. Yet, HLA-B27 exerts a negative effect on the level of this response, which could contribute to impaired defense against Yersinia.
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PMID:Cytotoxic T-cell-mediated response against Yersinia pseudotuberculosis in HLA-B27 transgenic rat. 1041 37

Reactive arthritis is one of the spondyloarthropathy family of clinical syndromes. The clinical features are those shared by other members of the spondyloarthritis family, though it is distinguished by a clear relationship with a precipitating infection. Susceptibility to reactive arthritis is closely linked with the class 1 HLA allele B27; it is likely that all sub-types pre-dispose to this condition. The link between HLA B27 and infection is mirrored by the development of arthritis in HLA B27-transgenic rats. In this model, arthritis does not develop in animals maintained in a germ-free environment. Infections of the gastrointestinal, genitourinary and respiratory tract appear to provoke reactive arthritis and a wide range of pathogens has now been implicated. Although mechanistic parallels may exist, reactive arthritis is distinguished from Lyme disease, rheumatic fever and Whipple's disease by virtue of the distinct clinical features and the link with HLA B27. As in these conditions both antigens and DNA of several micro-organisms have been detected in joint material from patients with reactive arthritis. The role of such disseminated microbial elements in the provocation or maintenance of arthritis remains unclear. HLA B27-restricted T-cell responses to microbial antigens have been demonstrated and these may be important in disease pathogenesis. The importance of dissemination of bacteria from sites of mucosal infection and their deposition in joints has yet to be fully understood. The role of antibiotic therapy in the treatment of reactive arthritis is being explored; in some circumstances, both the anti-inflammatory and anti-microbial effects of certain antibiotics appear to be valuable. The term reactive arthritis should be seen as a transitory one, reflecting a concept which may itself be on the verge of replacement, as our understanding of the condition develops. Nevertheless it appropriately describes arthritis that is associated with demonstrable infection at a distant site without traditional evidence of sepsis at the affected joint(s). Although several forms of disease could be described as "reactive", particularly acute rheumatic fever, post-meningococcal septicaemia arthritis and Lyme disease, in clinical practice the term is restricted to an acute spondyloarthritis, usually, but not exclusively, linked to acute genitourinary or gastrointestinal infection. A proportion of patients fulfil criteria for Reiter's Syndrome [1].
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PMID:Reactive arthritis. 1059 44

Four cases of reactive arthritis (ReA) related to Helicobacter pylori (HP) are presented. These were identified by IgG, IgM and IgA ELISA tests performed on sera obtained from a 2-year prospective study on 186 patients with a clinical picture suggesting ReA as a possible diagnosis. If anti-HP IgM and IgA or IgG were positive, the case was considered related to HP. Three out of four HP ReA patients were originally classified as "possible ReA", i.e. having a clinical picture of ReA but without any identified triggering microorganism. IgG antibodies against cagA and vacA were detected in three and two cases respectively. The HP ReA patients did not present with typical clinical or laboratory features differentiating them from ReA induced by Chlamydia trachomatis (N = 25) or enteropathogenic bacteria (N = 27). However, compared to findings in patients with ReA due to enteropathogenic bacteria the number of active joints was higher (six versus two), duration of arthritis longer (3.9 weeks versus 2 weeks) and the CRP (C-reactive protein) lower (43 versus 59). Our findings suggest that HP may be included in the list of possible arthritis triggering microbes.
Infection 1999
PMID:Helicobacter pylori--a trigger of reactive arthritis? 1088 36

The aim of the study was to assess if Szczecin voivodeship is an area of endemic borreliosis, assess the risk due to B. burgdorferi infection in habitants and evaluate clinical manifestations of borreliosis. The study was conducted in 1993-1995, material comprised 299 persons (211 men and 88 women) aged from 3 to 78 years, divided into two groups. Group I consisted of foresters working in four forestry districts, occupationally exposed to tick bite. Group II was completed of Szczecin voivodeship habitants, sporadically exposed to tick bite. Control group consisted of 30 healthy persons without exposure to tick bite. Research programme of study comprised epidemiologic data, clinical examination, evaluation of serum anti-B.b antibodies in all persons and assessment of some infectious parameters (red cells sedimentation--RCS, leukocytosis and C-Reactive Protein--CRP) during borreliosis. High prevalence of borreliosis was noted in both groups. Risk of borreliosis was similar in four forestry districts (Tab. 1). The hazard of infection was not restricted to forest areas only but was present in some parts of Szczecin and its suburbs (parks and gardens). Infection by B.b. was observed in both males and females in all age groups. Risk of B.b infection increased accordingly to duration of exposure but in some examined persons after single tick bite the disease developed (Tab. 2). Some of infected persons do not demonstrate clinical symptoms of borreliosis (Tab. 3). In most cases the disease was diagnosed in early stage of infection (Tab. 4). During infection different organs and systems were involved (Tab. 5). In clinical study skin was the most often affected organ followed by nervous system and joints (Tab. 5, 7). Clinical manifestations comprised erythema migrans chronicum, radiculitis, arthritis, meningitis, encephalitis and uveitis (Tab. 6). Serological study revealed the presence of serum anti-B.b antibodies in 47.6% of examined persons with occupational risk involving tick bite, and 32.7% persons of sporadic risk with negative serology of borreliosis in control group (Tab. 8). The parameters of acute inflammatory phase (RCS, CRP, leukocytosis) are of limited value in diagnosis of borreliosis.
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PMID:[Epidemiologic-clinical aspects of tick borne borreliosis in the Szczecin Province]. 1090 88

Primary immunodeficiency comprises a heterogeneous group of disorders. Autoimmune and/or rheumatic manifestations are not uncommon in these patients. It may be the first and/or sole sign before the underlying disease is established. This study focuses on the children of primary immunodeficiency with autoimmune disease to survey the clinical and laboratory finding retrospectively. From January 1985 to June 1998, ten patients (M:F = 9:1) of primary immunodeficiency with at least one well defined autoimmune disease were identified. The underlying immunodeficiency included three with Bruton's disease, three with common variable immunodeficiency, one with hyper-IgM, one with primary CD4 T-cell deficiency and two with Wiskott-Aldrich syndrome. The autoimmune manifestations include arthritis in six, ulcerative colitis in one, and autoimmune hemolytic anemia in three children. The major treatment was steroid and non-steroid anti-inflammatory drug. Infection could be controlled with antibiotics and intravenous immunoglobulin in all save one. The morbidity among these patients included bronchiectasis with pulmonary hypertension in three, joint stiffness, short stature, and delayed puberty in two. In conclusion, autoimmune diseases are frequently seen in patients with primary immunodeficiency. It could be the first and/or sole sign of disease. The possibility of immunodeficiency should be kept in mind when evaluating patients with autoimmune diseases.
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PMID:Autoimmune manifestations in patients with primary immunodeficiency. 1091 Jun 21

Although most joint pain in adolescents is secondary to injury, inflammatory arthritis, mechanical problems, and other causes, infectious causes of arthritis should always be considered. Infections may cause arthritis by direct infection, reactive disease, or immune-mediated mechanisms. This chapter reviews common infectious causes of arthritis and also recognizes the difficulties in distinguishing categories.
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PMID:Infectious causes of arthritis in adolescents. 1096 Dec 56


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