Do B cells influence disease progression in chronic synovitis? Lessons from primary hypogammaglobulinaemia.
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We describe a 62-yr-old male patient with primary hypogammaglobulinaemia (PH) who fulfilled the 1987 American Rheumatism Association/American College of Rheumatology revised diagnostic criteria for rheumatoid arthritis (RA) but, despite persistent symmetrical synovitis, did not develop erosions. Virology studies and blood and synovial fluid (SF) cultures were consistently negative; a search for crystals in the SF was unrevealing. Peripheral blood (PB) B cells were absent, whilst the PB CD3(+) cell count was normal. The ratio of naive (CD45RA(+)) to memory (CD45R0(+)) cells was also normal (1:1) but the CD4:CD8 ratio was reversed. To our knowledge, this is the first report which combines the immunophenotypic analysis of the PB with that of the SF and synovial membrane (SM). This confirmed the absence of B cells and the reversed CD4:CD8 ratio. However, as in other chronic arthropathies, the SF and SM cellular infiltrate consisted almost exclusively of memory T cells, consistent with the preferential localization of this subset to inflamed tissues. This case indicates that synovitis can proceed persistently in the absence of B cells and that the migratory mechanisms of T cells are not altered. However, the case suggests that the absence of B cells and negativity for rheumatoid factor, combined with an increased presence of CD8(+) (suppresser/cytotoxic) T cells in the joint, might contribute to the non-erosive nature of the synovitis. (+info)
An IFN-gamma-independent proinflammatory role of IL-18 in murine streptococcal cell wall arthritis.
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IL-18 is a member of the IL-1 family of proteins that exerts proinflammatory effects. It was formally known as IFN-gamma-inducing factor and is a pivotal cytokine for the development of Th1 responses. Apart from Th1 immune-stimulatory activity, IL-18 induces the production of proinflammatory cytokines such as TNF-alpha and IL-1 in vitro. The goal was to investigate the role of endogenous IL-18 in murine streptococcal cell wall (SCW)-induced arthritis. Furthermore, we investigated whether IL-18 neutralization had an impact on local TNF and IL-1 production. C57BL/6, BALB/c, and IFN-gamma-deficient mice were injected with 2 mg of rabbit anti-murine IL-18 Abs shortly before induction of arthritis by intra-articular injection of 25 microg of SCW fragments into the right knee joint. Suppression of joint swelling was noted on days 1 and 2 of SCW arthritis after blockade of endogenous IL-18. Analysis of local cytokine concentrations showed that IL-18, TNF-alpha, and IL-1ss levels were decreased. Severe inhibition of chondrocyte proteoglycan synthesis was seen in the vehicle-treated control animals, whereas a reversal of the inhibition of chondrocyte proteoglycan synthesis was found in the anti-IL-18-exposed animals. Blockade of endogenous IL-18 in IFN-gamma-deficient mice showed results similar to those found in wild-type animals, identifying a role for IL-18 that is IFN-gamma independent. The present study indicates that IL-18 is a proinflammatory cytokine during the onset of murine SCW arthritis, and this inflammatory role of IL-18 is IFN-gamma independent. (+info)
Bartonella infection associated with systemic juvenile rheumatoid arthritis.
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A 4-year-old girl with systemic juvenile rheumatoid arthritis had Bartonella infection diagnosed serologically. This case suggested that Bartonella (most probably Bartonella henselae) infection may in part be responsible for the development of systemic juvenile rheumatoid arthritis. (+info)
Septic arthritis of the hip associated with atopic dermatitis. A case report.
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We report a case of septic arthritis of the hip associated with atopic dermatitis. A 15-year female felt a pain in the right hip with unknown cause on May 11, 1998. The pain subsequently became aggravated, and she was admitted to our hospital on May 18. She has had atopic dermatitis since 4 years of age. She showed generalized dermatitis with desquamation and numerous scratch marks. A culture of both skin and joint fluid revealed Staphylococcus aureus. Physical examination revealed tenderness in Scarpa triangle and restricted range of motion. Immunological serology showed an increase in eosinophils and immunoglobulin E, and a decreased reaction of lymphocyte blastoid transformation. Computed tomography (CT) and MRI showed a joint effusion in the right hip. She was diagnosed as having septic arthritis of the hip. Intravenous drip of Cefazolin of 2g was started on the first day of hospitalization and joint irrigation was done on the second day. CRP became negative at 4 weeks, but joint effusion was shown on CT. Additional joint irrigation with Amicamycin (200 mg) was done. As the joint fluid culture became negative, range of motion exercises were started at 6 weeks. She was discharged with a long-leg brace applied at 8 weeks. At 13 months after onset, she had complete relief of the pain and normal activities of daily living. No destructive changes in the hip were found on X-ray examination or MRI. In the present case, an abnormal immune system associated with atopic dermatitis as well as the habit of scratching eruptions may have led to hematogenous spread of skin infection, and caused septic arthritis of the hip. (+info)
Severity of group B streptococcal arthritis in selected strains of laboratory mice.
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The susceptibilities of C3H/HeN, BALB/c, and C57BL/6N mouse strains to group B streptococci (GBS) infection were evaluated. C3H/HeN mice developed severe polyarthitis; mild lesions and no lesions were observed in BALB/c and C57BL/6N mice, respectively. A correlation between the severity of arthritis, the number of GBS in the joints, and local interleukin-6 and interleukin-1beta production was evident. (+info)
The diagnostic value of streptococcal serology in early arthritis: a prospective cohort study.
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OBJECTIVE: To evaluate the diagnostic value of streptococcal serology in adult early arthritis patients in discriminating between post-streptococcal reactive arthritis (PSRA) and arthritis with other causes. METHODS: The antistreptolysin-O (ASO) and anti-DNase B tests were performed at baseline in 366 consecutive, newly referred early arthritis patients. After 1 yr of follow-up the patients were classified according to international classification criteria and were evaluated for the presence of persistent arthritis. The outcome measures were the predictive value of streptococcal serology for the diagnosis of PSRA and the ability of this serology to discriminate at the first visit between the self-limiting and persistent forms of arthritis. RESULTS: With a positive serological result, the probability of having PSRA increased from 2 to 9%, whereas the probabilities of having rheumatoid arthritis or undifferentiated arthritis continued to be high (23 and 29%). The serological tests did not discriminate between the self-limiting and persistent forms of arthritis. The major Jones criteria apart from arthritis were not observed. CONCLUSION: Streptococcal serology has no diagnostic value in adult early arthritis patients in whom major Jones criteria other than arthritis are not present. (+info)
Regulatory effects of interleukin-4 and interleukin-10 on human neutrophil function ex vivo and on neutrophil influx in a rat model of arthritis.
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OBJECTIVE: To assess the capacity of interleukin-4 (IL-4) and IL-10 to block polymorphonuclear neutrophil (PMN) activation in an ex vivo human model system, and to confirm their effect on neutrophil function in an animal model of arthritis. METHODS: The ex vivo phagocytic capacity of cytokine-activated human PMNs was assessed by use of assays for measuring the ingestion of heat-killed yeast and by subsequent hexose-monophosphate shunt activation using nitroblue tetrazolium reduction. The in vivo activity of IL-4 and IL-10 was measured using a rat adjuvant arthritis model in which the mycobacterial antigen concentration was titrated to modify disease intensity. RESULTS: IL-4 and IL-10 suppressed the ex vivo activation state of interferon-gamma- and tumor necrosis factor alpha-activated human neutrophils. In the rat adjuvant arthritis model, treatment with systemic murine IL-10 (mIL-10) effectively suppressed all disease parameters in rats that received the lower concentrations of mycobacteria, whereas systemic mIL-4 was effective against even the most severe disease. Both cytokines were effective in lowering the absolute PMN cell number recovered and the PMN activation state in the joint synovia. We also observed lower levels of the messenger RNA transcript for CINC protein (cytokine-induced neutrophil chemoattractant; a rat homolog for human IL-8) in the synovia. CONCLUSION: IL-10 is an effective antiarthritic agent and has a major effect on the presence and function of PMNs in the joint synovia when disease intensity is not severe. IL-4 has an inhibitory profile that is similar to that of IL-10, but is effective in modifying even the most severe disease. Both cytokines reduced the phagocytic activation of human PMNs in response to proinflammatory cytokines. These data demonstrate that IL-4 and IL-10 can exert powerful regulatory effects on neutrophil function that translate into a therapeutic response in a disease model of arthritis. Treatment with these cytokines alone or in combination may therefore be very useful in the management of patients with rheumatoid arthritis. (+info)
Influence of interferon-gamma administration on the severity of experimental group B streptococcal arthritis.
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OBJECTIVE: To assess the effect of interferon-gamma (IFNgamma) administration on the evolution of systemic infection and septic arthritis induced by group B streptococci (GBS) in mice. METHODS: CD1 mice were inoculated intravenously with arthritogenic strain 1/82 of type IV GBS. Exogenous murine IFNgamma or anti-IFNgamma monoclonal antibodies were administered intravenously either 2 hours (-2 hours) before or 18 hours after infection with 1 x 10(7) GBS. Mice were monitored daily for survival and for signs of arthritis. In a subsequent set of experiments, mice were killed at selected times for examination of bacterial clearance, joint histopathology, and cytokine production. RESULTS: Mortality in mice treated with IFNgamma at -2 hours was 100%, compared with 20% in those treated at 18 hours and with 40% in controls. As indicated by the arthritis score, mice treated with IFNgamma at -2 hours developed early and more severe arthritis, whereas those treated at 18 hours had milder arthritis compared with infected controls. Less severe joint pathology in the mice treated with IFNgamma at 18 hours correlated with low levels of interleukin-6 (IL-6) and IL-1beta and a low bacterial load in the joints, whereas rapid onset and worsening of articular lesions in those treated at -2 hours corresponded to early and sustained levels of IL-6. CONCLUSION: The findings of this study demonstrate that the effects mediated by IFNgamma on GBS-induced arthritis may be detrimental or beneficial, depending on the time of administration of IFNgamma in relation to infection with the antigen. (+info)