Peripheral blood monocytes from patients with reactive arthritis show normal production of tumour necrosis factor-alpha.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Repo.
Explore the source record for details and available documents.
Oxygen derived free radicals are considered to play an important part in the development of inflammation. A whole blood chemiluminescence assay was used to study N-formyl-methionyl-leucyl-phenylalanine induced oxygen radical production in subjects with ankylosing spondylitis or previous yersinia arthritis. In luminol enhanced chemiluminescence, the subjects with previous yersinia arthritis showed significantly increased initial activation (at one minute), whereas the subjects with ankylosing spondylitis showed decreased responses at both the initial activation and at peak activation (at two to three minutes). This finding gives credence to the view that, in terms of oxygen radical production, the pathogenesis of yersinia arthritis is different from that of ankylosing spondylitis.
Explore the source record for details and available documents.
We studied functions of polymorphonuclear leucocytes (PMN) and monocytes from peripheral blood of subjects with familial hypercholesterolaemia (FH). FH monocytes exposed to Escherichia coli lipopolysaccharide (LPS) in 10% human AB serum generated tumour necrosis factor (TNF) significantly more than did control monocytes. After lowering of serum low-density lipoprotein (LDL) levels by drug treatment, FH monocytes exposed to LPS in the absence of exogenous lipoproteins generated significantly more TNF than did control monocytes. These findings suggest that increased TNF production is not affected by hypolipidaemic treatment and may not derive from differences between uptake of exogenous LDL by FH monocytes and control cells. Chemotaxis, chemokinesis, and random migration of both FH PMN and FH monocytes were normal, as determined by agarose assay and membrane filter assay. FH PMN showed increased luminol-enhanced chemiluminescence in response to 2.5 x 10(-8) M, but not to 2.5 x 10(-6) M, N-formyl-methionyl-leucyl-phenylalanine, and not to serum-treated zymosan or to phorbol myristate acetate. Luminol- and lucigenin-enhanced chemiluminescence responses of FH monocytes were normal. In summary, the major aberration found in the present study was that FH monocytes stimulated with LPS show enhanced production of TNF. The possibility that exaggerated TNF production contributes to an early development of atherosclerotic lesions in FH subjects warrants further studies.
We studied the chemotaxis of peripheral blood polymorphonuclear leukocytes (PMNs) and monocytes and the production of tumor necrosis factor alpha by monocytes of patients with juvenile periodontitis (JP). As a group, the patients' PMNs showed significantly increased chemotaxis determined by counting the number of migrating cells within a 3-microns-pore-size filter. Determined as distance of migration within the filter, as chemotactic increment based on checkerboard analysis, as leukotactic index calculated on the basis of distance of migration and cell count at different depths within a 3-microns-pore-size filter, as distance of migration under agarose, and as the number of PMNs migrating across a 5-microns-pore-size filter, the chemotactic migration rates of PMNs of patients were similar to those of controls. Evaluation of the data on an individual basis suggested that in terms of PMN chemotaxis some patients were hyperresponsive and some were hyporesponsive. Chemotaxis, spontaneous migration, and the rates of lipopolysaccharide-induced tumor necrosis factor alpha production by JP monocytes were similar to those of control cells. Our results give credence to the view that there are minor aberrations in the functions of JP phagocytes, but the extent to which these aberrations are relevant to accumulation of PMNs at sites of infection and inflammation in vivo and possibly contribute to the pathogenesis of JP remains unclear.
The chemotaxis and chemiluminescence responses of polymorphonuclear leucocytes (PMN) of synovial fluid and peripheral blood from patients with acute reactive arthritis were studied. Rates of chemotactic and chemokinetic migration of synovial fluid PMN were significantly decreased. In addition, chemiluminescence responses tended to be depressed, suggesting that the cells were deactivated for both chemotaxis and production of oxygen derived free radicals. Such deactivation has been described previously as a characteristic of synovial fluid PMN in rheumatoid arthritis. Compared with those with a mild disease, patients with severe acute reactive arthritis had higher chemiluminescence responses of synovial fluid PMN to phorbol myristate acetate during acute disease and developed increased migration of peripheral blood PMN towards zymosan treated serum after recovery from the disease. This supports the view that hyperreactive PMN contribute to the development of severe inflammatory symptoms in acute reactive arthritis.
Pathogenesis of seronegative spondyloarthropathies such as ankylosing spondylitis and reactive arthritis is not known. Growing evidence indicates that microbial structures such as Chlamydia antigen and Yersinia antigen are present in the inflamed joints of patients with reactive arthritis. Microbial antigens can activate the host's inflammatory mechanisms. After the activation, the course of inflammation can be postulated to be affected by the host factors responsible for amplification of the inflammatory reaction and elimination of the foreign structures. Thus, the amplification, whether strong, moderate, or weak, may contribute to the degree of inflammatory tissue injury in patients with seronegative spondyloarthropathies. This review will discuss the role of increased inflammatory reactivity in the pathogenesis of HLA-B27 associated spondyloarthropathies, with special reference to reactive arthritis triggered by yersinia enteritis.
Explore the source record for details and available documents.
In countries where malaria is not endemic the diagnosis of the disease is often delayed or overlooked, particularly if the clinical symptoms are atypical and if automated cell analyzers are used instead of blood films for leucocyte differential counts. We report 2 cases of severe Plasmodium falciparum malaria with unusual clinical features: a 46-year-old man with an exceptionally long incubation period and a 22-year-old woman with presenting symptoms suggesting viral hepatitis. In both cases the diagnosis of malaria was unexpectedly made by observant laboratory technicians examining stained blood films for differential counts.
We studied the effects of different variables on luminol-enhanced chemiluminescence (CL) of whole blood, induced by N-formyl-methionyl-leucyl-phenylalanine (FMLP), opsonized zymosan particles (OZP), or phosphate buffered saline (PBS). Use of correction factor based on blood neutrophil count and hemoglobin concentration decreased interindividual variation and improved normality of the frequency distributions of CL responses. In FMLP- and PBS-induced CL, day-to-day variation was not significant, but it was significant in OZP-induced CL. Although storage of blood samples for 8 hours decreased CL, the decrease was not evident in a study of initial activation, i.e. CL measured at one minute after application of FMLP. Our results suggest that FMLP-induced initial activation is well suited for epidemiological studies because it is easy to determine and is affected neither by day-to-day variation nor by storage of the blood samples for a few hours.
During a seven-year period we observed 14 children who had chronic osteomyelitislike disease. The bacterial cultures from the bone lesions were negative. In eight patients the findings were compatible with chronic recurrent multifocal osteomyelitis (CRMO), in four the findings were compatible with chronic sclerosing osteomyelitis of Garré, and two had osteomyelitis of the clavicle. In patients with CRMO, lymphocyte subpopulations, the responses to mitogens, and the chemotactic and chemokinetic responses showed no consistent abnormalities. After a mean follow-up of 4.5 years (range, one to ten years), all four patients with osteomyelitis of Garré were symptomatic, and two had complications. Only two of the eight patients with CRMO had active disease. The course had been complicated by growth disturbances in one patient and by thoracic outlet syndrome in another. Wegener's granulomatosis later developed in a patient with CRMO.
Several studies have failed to show an association between Shigella sonnei dysentery and reactive arthritis. We describe 3 patients who had reactive arthritis and a recent or concurrent S sonnei infection. To our knowledge, this is only the second study to suggest this association. We propose that S sonnei should be considered as a triggering agent for reactive arthritis.
PURPOSE: In order to evaluate the relationship between cachectin/tumor necrosis factor (TNF) and cachexia in the acquired immunodeficiency syndrome (AIDS), we studied the serum levels of endogenous cachectin/TNF in subjects with human immunodeficiency virus (HIV) infection. PATIENTS AND METHODS: Fifty-three serum samples were obtained from 39 HIV-seropositive patients. The condition of each patient was clinically classified as either asymptomatic, lymphadenopathy syndrome (LAS), AIDS-related complex (ARC), or AIDS. Control sera were obtained from 29 healthy male blood donors. A double antibody radioimmunoassay was used to measure the serum levels of cachectin/TNF. RESULTS: Cachectin/TNF levels were within the reference range of the control values in all (eight of eight) asymptomatic HIV-infected subjects and in 11 of 13 of the patients with LAS. In contrast, all patients with AIDS (nine of nine) and five of nine of the patients with ARC had raised levels of cachectin/TNF. Fluctuation of the levels of cachectin/TNF occurred during follow-up, but initially raised levels remained elevated. CONCLUSION: Since cachectin/TNF suppresses lipoprotein lipase in adipocytes in vitro, and causes weight loss under experimental conditions, the findings of raised levels of cachectin/TNF in patients with AIDS may have relevance to the pathogenesis of cachexia.
The efficiency of complement activation was studied in sera from HLA-B27 positive and negative subjects (27 with previous yersinia arthritis and 35 controls). Activation of complement with zymosan induced higher mean levels of the anaphylatoxin C3a in HLA-B27 positive sera (mean (SD) 7.40 (1.66) mg/l) than in HLA-B27 negative sera (6.41 (1.79) mg/l). Similarly, higher levels of C3d,g, another C3 breakdown fragment, were obtained in HLA-B27 positive sera after Escherichia coli 0111:B4 lipopolysaccharide treatment (17.6 (3.7)% v 15.0 (3.8)%). The differences occurred irrespective of previous arthritis, complement C4 or Bf phenotype, or variation in background complement levels. The findings suggest that an increased responsiveness to complement activators may contribute to the pathogenesis of HLA-B27 associated inflammatory diseases.
Polymorphonuclear leucocyte (PMN) functions (migration in vitro, chemiluminescence, O-2 production, and aggregation) were studied in 32 patients with previous yersinia arthritis (YA). PMNs of 11 HLA-B27 positive patients who had chronic or recurrent inflammatory symptoms showed O-2 production significantly higher than that of PMNs of 11 HLA-B27 positive patients without late manifestations. Also, PMNs of both HLA-B27 positive and negative patients tended to show chemotactic and chemokinetic migration rates higher than those of control cells of healthy HLA-B27 negative subjects. These functional aberrations may play a part in the development of the patients' inflammatory symptoms.
We describe a patient, a 59-year-old woman, who developed erythema nodosum and conjunctivitis after enteritis due to Salmonella typhimurium. The patient was HLA-B27 negative and had circulating immune complexes, as determined by the conglutinin-binding enzyme immunoassay. Immunopathogenesis of the extraintestinal findings is discussed.