Release of Prostaglandin‐like Substances by Shigella Endotoxin and Its Inhibition by Non‐steroidal Anti‐inflammatory Compounds

Bhattacherjee, P.

doi:10.1111/j.1476-5381.1975.tb07595.x

Cited by 56 publications

(13 citation statements)

References 33 publications

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“…Other investiga tors have also noted the presence of certain AA metabolites in animal models of experi mental intraocular inflammation, as well as in inflamed human ocular tissues. PG-like substances were found to be increased in rabbits following intravitreal administration of Escherichia coli endotoxin, M. butyricum [17], Shigella endotoxin [18] or bovine se rum albumin [19], PG-like activity was also detected in aqueous humor samples of pa tients with acute uveitis [20]. The levels of the material correlated well with the inten sity of uveitis as determined clinically.…”

Section: Discussionsupporting

confidence: 50%

Treatment of S Antigen Uveoretinitis with Lipoxygenase and Cyclo-Oxygenase Inhibitors

Chen¹,

Pararajasegaram²,

Sevanian³

et al. 1991

Ophthalmic Res

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The role of metabolites of arachidonic acid (AA) in experimental autoimmune uveoretinitis was studied using inhibitors of AA metabolism. Nordihydroguaiaretic acid (NDGA), which inhibits predominantly the lipoxygenase (LO) pathway, or indomethacin, a specific cyclo-oxygenase (CO) inhibitor, was administered to rats imunized with retinal S antigen. Levels of various AA metabolites were measured in the inflamed uvea, and the severity of intraocular inflammation was quantitated by morphometric analysis. Histopath-ologically, the uveoretinitis was significantly suppressed following treatment with NDGA, while indomethacin treatment resulted in augmentation of the disease (p < 0.05). These results tend to indicate that the inhibition of the LO rather than the CO pathway may be more beneficial in the treatment of autoimmune uveitis.

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Section: Discussionsupporting

confidence: 50%

Treatment of S Antigen Uveoretinitis with Lipoxygenase and Cyclo-Oxygenase Inhibitors

Chen¹,

Pararajasegaram²,

Sevanian³

et al. 1991

Ophthalmic Res

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“…A predominantly inflammatory role for IL-6 is a logical conclusion based upon several relationships observed between endotoxin and cytokines ; i.e. endotoxin induces uveitis (Bhattacherjee, 1975 ;Rosenbaum et al, 1980), endotoxin works largely through induction of IL-1 and TNF-α (Beutler and Cerami, 1987 ;Dinarello, 1991), and IL-1 and TNF-α are potent agonists for IL-6 production (Akira et al, 1990 ;Gimble et al, 1991 ;Littlewood et al, 1991 ;Sironi et al, 1989). Furthermore, IL-6 levels increase in intraocular fluids during episodes of intraocular inflammation (Limb et al, 1991 ;Murray et al, 1990 ;Norose et al, 1994) and intravitreally injected IL-6 induces uveitis in Lewis rats (Hoekzema et al, 1991(Hoekzema et al, , 1992.…”

Section: Discussionmentioning

confidence: 95%

Rabbit Pigmented Ciliary Epithelium Produces Interleukin-6 in Response to Inflammatory Cytokines

Fleisher

McGahan

Ferrell

2000

Experimental Eye Research

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“…Endotoxins, which are lipopolysaccharides located in the walls of Gram negative bacteria, are also capable of inducing synovial inflammation (19). Others have described stimulation of prostaglandin synthesis by endotoxins in experimental animals (20,21). Present results indicate that endotoxins stimulate the production of both PGE and HA synthesis by cultured human synovial fibroblasts.…”

Section: Discussionmentioning

confidence: 99%

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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Release of Prostaglandin‐like Substances by Shigella Endotoxin and Its Inhibition by Non‐steroidal Anti‐inflammatory Compounds

Cited by 56 publications

References 33 publications

Treatment of S Antigen Uveoretinitis with Lipoxygenase and Cyclo-Oxygenase Inhibitors

Treatment of S Antigen Uveoretinitis with Lipoxygenase and Cyclo-Oxygenase Inhibitors

Rabbit Pigmented Ciliary Epithelium Produces Interleukin-6 in Response to Inflammatory Cytokines

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

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