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T Bremell

Publications and source records attributed to T Bremell.

29 records · Page 2Linked to original sources
PubMed1994

Role of T lymphocytes in experimental Staphylococcus aureus arthritis.

Using a recently developed murine model of haematogenously induced Staphylococcus aureus, the authors have characterized the phenotypes and functional properties of inflammatory cells present in the synovium of arthritic mice. The results show that large numbers of granulocytes and macrophages were observed in the inflamed synovia within 24 h of inoculation of S. aureus strain LS-1. Many of the synovial macrophage-like cells strained for cytoplasmic IL-1 alpha and TNF-alpha. Subsequently (> or = 48 h later), a prominent infiltration of T lymphocytes, predominantly of CD4+ phenotype, was observed. Some of the T lymphocytes stained for IL-2 receptor and intracytoplasmic interferon-gamma (IFN-gamma). Surprisingly, in spite of the severe inflammatory process, very few cells expressed MHC class-II molecules in the arthritic synovia. In addition, in vivo depletion of CD4+ T-cells resulted in a considerably milder course of staphylococcal arthritis. The similarities in the phenotype expression of synovial cells and central role of T-cells in S. aureus arthritis as well as in non-infectious models of arthritis, indicate that the process governing joint destruction is likely to be the same, irrespective of the initial stimulus.

Animals↗
PubMed1994

The Staphylococcus aureus collagen adhesin is a virulence determinant in experimental septic arthritis.

The importance of a collagen-binding adhesin in the pathogenesis of septic arthritis has been examined by comparing the virulence of two sets of Staphylococcus aureus mutants in an animal model. Collagen adhesin-negative mutant PH100 was constructed by replacing the chromosomal collagen adhesin gene (cna) in a clinical strain, Phillips, with an inactivated copy of the gene. Collagen adhesin-positive mutant S. aureus CYL574 was generated by introducing the cna gene into CYL316, a strain that normally lacks the cna gene. Biochemical, immunological, and functional analyses of the generated mutants and their respective parent strains showed that binding of 125I-labeled collagen, expression of an immunoreactive collagen adhesin, and bacterial adherence to cartilage were directly correlated with the presence of a functional cna gene. Greater than 70% of the mice injected with the Cna+ strains developed clinical signs of arthritis, whereas less than 27% of the animals injected with Cna- strains showed symptoms of disease. Furthermore, mice injected with the Cna+ strain Phillips had remarkably elevated levels of immunoglobulin G1 and interleukin-6 compared with mice injected with the Cna- mutant PH100. Taken together, these results demonstrate that collagen adhesin plays an important role in the pathogenesis of septic arthritis induced by S. aureus.

Adhesins, Bacterial↗
PubMed1994

Protective role of sialophorin (CD43)-expressing cells in experimental Staphylococcus aureus infection.

Sialophorin (CD43) is a major surface mucin on most hematopoietic cell lineages, including phagocytes. Defects of CD43 expression occur in Wiskott-Aldrich syndrome, a disease characterized by susceptibility to pyogenic infections. In a newly established rat model of septic Staphylococcus aureus arthritis, we have investigated the role of CD43-expressing cells in the progression of the disease. A single injection of a monoclonal antibody specific for CD43 induced a highly erosive course of arthritis and increased mortality in animals exposed to a suboptimal dose of bacteria. Our results demonstrate that sialophorin-expressing cells play a protective role in the early stage of staphylococcal infection.

Animals↗
PubMed1994

Immunopathological features of rat Staphylococcus aureus arthritis.

Staphylococcus aureus is the most common bacterial species found in nongonococcal bacterial arthritis in humans. We present the first description, to our knowledge, of an outbreak of spontaneous staphylococcal arthritis in a rat colony. In a group of 10 rats, 9 displayed arthritis. Clinically, the most obvious findings were arthritis of one or both hindpaws and malaise. Bacteriophage typing showed the common phage type 85 in isolates recovered from the joints, blood, and bedding of rats and from the nose and cheeks of one person from the staff of the animal facility. The S. aureus strain proved to produce staphylococcal enterotoxin A and exhibited strong binding to collagen types I and II and bone sialoprotein, which are potentially important virulence factors. When the recovered S. aureus strain was injected intravenously into healthy rats, severe septic arthritis was induced in almost all of the animals. The arthritic lesions were characterized by infiltration of phagocytic cells and T lymphocytes into the synovium. Many of the synovial cells strongly expressed major histocompatibility complex class II molecules. Increased levels of interleukin 6 in serum as well as a prominent polyclonal B-cell activation were noted throughout the disease course. Pretreatment of S. aureus-injected rats in vivo with an antibody to the alpha beta T-cell receptor significantly decreased the severity of the arthritis. Our results indicate that alpha beta + T lymphocytes contribute to an erosive and persistent course of S. aureus arthritis.

Animals↗
PubMed1993

The accessory gene regulator (agr) controls Staphylococcus aureus virulence in a murine arthritis model.

We have studied the role of the accessory gene regulator (agr) of Staphylococcus aureus as a virulence determinant in the pathogenesis of septic arthritis. At least 15 genes coding for potential virulence factors in Staphylococcus aureus are regulated by a putative multicomponent signal transduction system encoded by the agr/hld locus. agr and hld mutants show a decreased synthesis of extracellular toxins and enzymes, such as alpha-, beta-, and delta-hemolysin, leucocidin, lipase, hyaluronate lyase, and proteases, and at the same time an increased synthesis of coagulase and protein A as compared with the wild-type counterpart. We have used a recently described murine model of S. aureus-induced arthritis to study the virulence of S. aureus 8325-4 and two agr/hld mutants derived from it. Sixty percent of the mice injected with the wild-type strain developed arthritis, whereas agrA and hld mutants displayed joint involvement in only 10 and 30%, respectively. In addition, 40% of the mice inoculated with the wild-type strain displayed an erosive arthropathy; such changes were not detectable at all in mice inoculated with the agrA mutant. Serum levels of interleukin-6, a potent B-cell differentiation factor, were significantly higher (P < 0.001) in the mice inoculated with the wild-type strain than in those inoculated with the agrA mutant counterpart. Overall, our results suggest that the agr system of S. aureus is an important virulence determinant in the induction and progression of septic arthritis in mice.

Animals↗
PubMed1992

Histopathological and serological progression of experimental Staphylococcus aureus arthritis.

In a newly developed mouse model of Staphylococcus aureus arthritis the kinetics of joint destruction and serological manifestations as well as the clinical course of arthritis and osteitis were studied. Almost all mice developed histopathological signs of arthritis upon a single intravenous injection of 10(7) S. aureus LS-1 cells. There was rapid joint destruction, with synovial hypertrophy already visible, within 24 h after injection of the bacteria. Cartilage and/or bone erosions were seen in a majority of the mice within 72 h. Extra-articular manifestations, especially signs of bone infection, were also found soon after inoculation of the bacteria. Tail osteitis was frequent (50% of the mice) but appeared later than arthritis. Polymorphonuclear cells prevailed in the early joint lesions and were also common in the extra-articular manifestations. Within 3 days, mononuclear cells were also seen in the inflamed synovium, gaining a dominant position 3 weeks after the start of the disease. Serum interleukin-6 levels were already increased within 6 h after bacterial injection and remained elevated throughout the course of arthritis. Serum tumor necrosis factor levels were increased within 24 h. There was a tremendous induction of immunoglobulin production, especially of the immunoglobulin G1 isotype. This was paralleled by the production of specific antibodies to S. aureus (cell walls and toxin), as well as autoantibodies (rheumatoid factors and anti-single-stranded DNA antibodies), all predominantly of the immunoglobulin G isotype. The type and magnitude of the immunoglobulin G response together with the elevated interleukin-6 levels speak in favor of both antigen-specific and polyclonal B-cell activation during S. aureus arthritis. This study points out important similarities between our new model of S. aureus arthritis and human S. aureus arthritis. This resemblance will enable controlled studies of pathogenetic mechanisms of septic arthritis as well as therapeutic and prophylactic approaches.

Animals↗
PubMed1991

Experimental Staphylococcus aureus arthritis in mice.

Staphylococcus aureus arthritis is usually caused by bacteremia and is highly destructive. Controlled studies on septic arthritis in humans are difficult to perform, because the time of onset of the infection is unknown. Animal models of bacterial arthritis make it possible to control important variables in experimental studies. We present a mouse model of S. aureus arthritis in which the intravenous administration of 10(7) cells of S. aureus LS-1 induced arthritis or osteitis or both within 3 weeks in 80 to 90% of the mice. Signs of arthritis emerged within the first few days after the injection. An interesting finding was that the S. aureus strain used in this study binds bone sialoprotein, a glycoprotein known to be specifically localized to bone tissue. This new model of S. aureus arthritis enables the study of the kinetics of joint destruction and the host-bacterium relationship as well as therapeutical approaches to septic arthritis and osteomyelitis.

Animals↗
PubMed1991

Rheumatic symptoms following an outbreak of campylobacter enteritis: a five year follow up.

Eighty six of 106 (81%) guests attending a party were followed up after an outbreak of Campylobacter jejuni enterocolitis. Acute diarrhoeal illness was reported in 35 subjects (33%), of whom seven showed acute rheumatic symptoms either alone or with other symptoms of infection with C jejuni. The antibody response to C jejuni corresponded well with the intensity of the disease. In the early phase of the gastrointestinal disease the patients with acute rheumatic symptoms displayed significantly higher IgM antibody levels in serum samples than the other patients in this study. Levels of antibodies to C jejuni were increased in serum samples from 31 patients (29%) without symptoms of infection with C jejuni. At a follow up after five and a half years, four of these patients suffered from chronic rheumatic disorders. One HLA-B27 positive woman developed reactive arthritis with a relapse seven years later. The remaining 20 subjects (19%) remained healthy and their antibody tests and stool cultures were negative for C jejuni. It is concluded that C jejuni enterocolitis is significantly associated with rheumatic symptoms in the early phase and may also cause chronic rheumatic disorders.

Acute Disease↗
PubMed1990

Outbreak of spontaneous staphylococcal arthritis and osteitis in mice.

Staphylococcus aureus is the most common bacterial species found in association with nongonococcal bacterial arthritis in humans. We present here the first description of spontaneous bacterial arthritis and osteitis in mice. Clinically, the most obvious findings were swelling and/or ankylosis of hindpaws and nodose changes of the tail. The prevalence of arthritis and osteitis ranged from 0% to greater than 50% of the mice studied, depending on the mouse strain. The most prominent histopathologic feature of the arthritis was hypertrophy of the synovial tissue and destruction of cartilage and underlying bone. Most of the S aureus-infected mice displayed an identical phage type, which was also the only S aureus phage type found in skin isolates from clinically healthy mice. However, a few S aureus isolates were not typeable, indicating that an additional strain(s) might cause bacterial arthritis in mice.

Animals↗
PubMed1983

Metatarsal head resection in the treatment of the rheumatoid forefoot.

When conservative treatment in the management of the painful rheumatoid forefoot fails, surgery should be advocated. The aim is to relieve the sole from pressure on the metatarsal heads, which causes callosities on and pain in the forefoot. Various surgical procedures have been described, but they have in common to replace or remove the fat pad under the metatarsal phalangeal joints, to resect the metatarsal heads and, in doing this, restore the metatarsal ends to a flat arc. For if the intermediate metatarsals are left too long, new pressure points may develop, with ensuing pain. In this investigation a 4 1/2-year follow-up is presented of 32 patients operated on with metatarsal head resection in 59 feet. Twenty-two patients representing 39 feet were very satisfied, whereas 8 patients representing 15 feet were dissatisfied. Walking ability improved considerably; standing on toes improved; muscle power of toes improved. Despite attempting to maintain the metatarsal arc as a flat curve, this proved to be uneven in 25 feet, but did not jeopardize the results. The complications were minor and did not influence the final results. These, however, were decidedly influenced by the functional class of the patient at the time for investigation. Surgical management of the painful rheumatoid forefoot appears to be a recommendable procedure.

Arthritis, Rheumatoid↗