The effect of bacterial products on synovial fibroblast function: hypermetabolic changes induced by endotoxin

Buckingham, Robert B.; Castor, C. William

doi:10.1172/jci106912

Cited by 42 publications

(14 citation statements)

References 21 publications

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“…Increased lactic acid production by synovium has been demonstrated in patients with inflammatory joint disease (12-13) and in response to extracts from gram-negative bacteria (14). Many of the short-chain fatty acids reported in this study are essential components of human metabolism.…”

Section: Discussionsupporting

confidence: 50%

Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis

Borenstein

Gibbs

Jacobs

1982

Arthritis & Rheumatism

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Nonvolatile short-chain fatty acids from 80 synovial fluids were quantified by gas-liquid chromatography. Succinic acid was detectable in all 23 septic synovia1 fluids infected with either gram-positive or gramnegative organisms and in only 5 of 57 nonseptic synovial fluids. Lactic acid was present in all of the effusions but was correlated with septic arthritis only when present in concentrations greater than 250 mg% .Neither short-chain fatty acid was more sensitive than high white blood cell counts (>50,000 mm3) or depressed glucose concentration (<40 mg/dl) in diagnosing septic arthritis before antibiotic therapy; however, the detection of succinic acid was helpful in identifying patients with septic arthritis who had been given antibiotic treatment before arthrocentesis. Thus, gas-liquid chromatography, a rapid and sensitive method for the detection of short-chain fatty acids, may complement the currently available methods used to diagnose septic arthritis.

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Section: Discussionsupporting

confidence: 50%

Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis

Borenstein

Gibbs

Jacobs

1982

Arthritis & Rheumatism

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“…Fibroblasts also demonstrate metabolic changes when cultured in the presence of LPS. Buckingham et al (16) showed that LPS stimulated synovial fibroblast hyaluronic acid production, glucose utilization, and lactate output. Recently, Yaron et al.…”

Section: Resultsmentioning

confidence: 99%

Bacterial lipopolysaccharides induce in vitro degradation of cartilage matrix through chondrocyte activation.

Jasin¹

1983

J. Clin. Invest.

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with LPS abolished matrix release, whereas Polymyxin B had no effect on the matrix-degrading activity provided by blood mononuclear cell factors. A highly purified Lipid A preparation induced matrix degradation at a concentration of 0.01 ug/ml. Cartilage matrix collagen and proteoglycan depletion also occurred with porcine articular cartilage explants (collagen release: 18.3±3.5%, medium control: 2.1±0.5%; proteoglycan release: 79.0±5.9%, medium control: 28.8±4.8%). Histochemical analysis of the cultured explants confirmed the results described above. Gel chromatography of the proteoglycans released in culture indicated that LPS induced significant degradation of the high molecular weight chondroitin sulfatecontaining aggregates.These findings suggest that bacterial products may induce cartilage damage by direct stimulation of chondrocytes. This pathogenic mechanism may play a role in joint damage in septic arthritis and in arthropathies

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“…Others have reported stimulation of hyaluronic acid induced by bacterial endotoxins in human synovial fibroblast cultures (7). We have recently reported an interrelationship between stimulation of hyaluronic acid (HA) and that of prostaglandin E (PGE) in human cultured synovial fibroblasts (8).…”

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confidence: 97%

Stimulation of prostaglandin e production by bacterial endotoxins in cultured human synovial fibroblasts

Yaron

Smetana

et al. 1980

Arthritis & Rheumatism

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E coli, shigella, salmonella, and cholera endotoxins stimulated prostaglandin E (PGE) production by cultured human synovial and foreskin fibroblasts. The minimal effective dose of Shigella endotoxin was 2 pg/ ml and a maximal response was observed at 10 pg/ml. PGE stimulation was first detected 7 hours after addition of cholera endotoxin. Stimulation by shigella endotoxin of both PGE and hyaluronic acid production was inhibited by indomethacin and aspirin. The present results suggest that PGE is a mediator of joint inflammation induced by endotoxins.A possible relationship between an infectious agent and joint inflammation has been repeatedly reported (1,2). It is possible that such an agent triggers an inflammatory process which in some cases is subsequently perpetuated by other factors (3). An intriguing observation, which has received no clear explanation, is the relationship between acute and chronic bowel diseases and arthritis (4). It is possible that endotoxins liberated from Gram negative bacteria in the bowel trigger an inflammatory reaction in the synovial membrane.There is ample evidence to suggest that prostaglandins are mediators of the inflammatory process (5,6). Others have reported stimulation of hyaluronic acid induced by bacterial endotoxins in human synovial fibroblast cultures (7). We have recently reported an interrelationship between stimulation of hyaluronic acid (HA) and that of prostaglandin E (PGE) in human cultured synovial fibroblasts (8). A preliminary study showed stimulation of both PGE and hyaluronic acid in human synovial fibroblast cultures by shigella endoThe present study reports the stimulation of prostaglandin E induced by different bacterial endotoxins in synovial and foreskin fibroblast cultures. MATERIALS AND METHODS toxin (9).Fibroblasts derived from synovial membranes obtained during meniscus tear operations of otherwise healthy persons were grown in monolayer cultures by methods previously reported by Castor et a1 (10). Human foreskin fibroblasts were obtained from Dr. Dalia Gurari-Rotman and Professor Michel Revel at the Weizmann Institute of Science, Israel. T-30 tissue culture flasks (5 ml of medium per flask) with siliconized rubber stoppers were inoculated with 0.5 X lo6 fibroblasts and incubated at 37OC. Synovial fibroblasts and HeLa cells were grown in medium CMRL 1066 (Gibco) (~W O ) , heat inactivated human serum (lo%), and fetal calf serum (lo%), supplemented with L-glutamine, penicillin, and streptomycin. Eagle's MEM (90%) with fetal calf serum (10%) was used for the foreskin monolayer cultures. "Purified" endotoxins (lipopolysaccharides) were purchased from Sigma

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The effect of bacterial products on synovial fibroblast function: hypermetabolic changes induced by endotoxin

Cited by 42 publications

References 21 publications

Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis

Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis

Bacterial lipopolysaccharides induce in vitro degradation of cartilage matrix through chondrocyte activation.

Stimulation of prostaglandin e production by bacterial endotoxins in cultured human synovial fibroblasts

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