<i>In vivo</i> effects of cellulose sulphate on plasma kininogen, complement and inflammation

Eisen, V.; Loveday, Clive

doi:10.1111/j.1476-5381.1971.tb07123.x

Cited by 20 publications

(8 citation statements)

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“…4). Ellagic acid is known to selectively deplete kininogen (CRUNKHORN and MEACOCK [9]), but carrageenin besides of depleting kininogen (EISEN and LOVEDAY [12]) has also been shown to suppress complement titres (WARD and COCHRANE [25]). Our results were thus indicative that the kininogen-kinin system is foremostly involved in the middle-phase of the hind-paw inflammation, while in the delayed phase complement is probably involved.…”

Section: Inhibition (~)mentioning

confidence: 99%

Anti-inflammatory mechanism of inflamed-tissue factor

Bonta

Noordhoek

1973

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The early postulation that irritation of tissue could release a substance which acted as anti-inflammatory agent at a remote site of the body, led further to show that administration of inflammatory exudate results in suppression of experimental inflammations (Rindani [22], Robinson and Robson [23], Billingham, Robinson and Robson [2], Bonta and De Vos [6]). Little is known however as to which type of inflammatory response is preferentially inhibited by inflammed-tissue factors(s) and even less is known about the mechanism associated with this inhibition. Earlier we studied the anti-inflammatory effect of exndates from peritoneal inflammation, but in later experiments we made use of exudates obtained from aircarrageenin granuloma pouches of rats (Bonta, Bhargava and De Vos [7]). The dialysate of the exudate showed only potency in suppressing the kaolin induced hind paw inflammation of the rat. A marked and dose dependent inhibition of this inflammation was however found with the retentate. The anti-inflammatory macromolecaiar (mol wt 200,000) portion of the exudate is a complexity of proteins and may be other materials. The macromolecular factor(s) obtained from donor rats did also suppress the kaolin induced hind paw inflammation when administered to mice, herewith ruling out species-specificity. The antiinflammatory effect of the exudate was not diminished by adrenalectomy of the test-animals, thus excluding the discharge of corticosteroids as a conceivable mechanism. The macromolecular retentate did not only cause inhibition of the kaolin induced inflammation, but the carrageenininflammation in rats was also suppressed. On the other hand the inflammatory response by histamine or serotonin was not inhibited by the pouch-exudate, which thus apparently displays a preferential inhibition of certain type of inflammations while leaving others unaffected (Bonta, Bhargava and De Vos [7]). We found no indications that the anti-inflammatory effect of the exudate factor(s) was mediated through either influencing the kininogen-kinin system or interfering with prostaglandins as putative inflammatory mediators. However depletion of complement was evident in the carrageenin induced inflammation, representing the type of response which is sensitive to the anti-inflammatory effect by the pouchexudate. In line with this we have data that the exudate inhibits total complement activity of serum when either added in vitro or administered in vivo. The complement inhibitory property of the exudate seemed to parallel with the anti-inflammatory activity. Complement fixation has been proposed as the underlying mechanism of the counterirritant principle (Willoughby, Coote and Turk [26]), which in fact was the early starting point to investigate the anti-inflammatory effect of exudates obtained from irritated tissue. It is however not likely that tissue irritation due to injection of our macromolecnlar factor is the exclusive mode in its anti-inflammatory effect. In fact we observed the anti-inflammatory effect even after intra...

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Section: Inhibition (~)mentioning

confidence: 99%

Anti-inflammatory mechanism of inflamed-tissue factor

Bonta

Noordhoek

1973

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“…It has been shown that cellulose sulphate (Rothschild, 1967(Rothschild, , 1968Eisen & Loveday, 1971), activates plasma arginine-ester esterase and depletes plasma kininogen in rat, guinea-pig and man, releasing kinins. In addition, Rothschild (1968) observed that following injection of cellulose sulphate, fibrinolytic activity appears in rat's plasma.…”

Section: Introductionmentioning

confidence: 99%

Fibrinolytic activity evoked in the plasma of the normal and adrenalectomized rat by cellulose sulphate

Rosa

Rothschild

1972

British J Pharmacology

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Summary1. Cellulose sulphate, a kinin-releasing agent, produced fibrinolytic activity in plasma when administered intravenously to the rat but not when added to fresh rat plasma in vitro. The in viva effect was maximal within 1 min and disappeared within 10-20 minutes. It was retained in plasma taken 1 min after the injection and kept at room temperature for 30 minutes. 2. A decrease of anti-fibrinolytic potency measured against urokinaseactivated bovine plasmin, was shown to occur in plasma of rats given cellulose sulphate. 3. Activated rat plasma lysed heat-denatured fibrin: it probably contains free plasmin as well as plasminogen activator. 4. Adrenalectomized rats did not exhibit fibrinolytic activity nor statistically significant benzoyl-arginine ethyl ester-esterase activation in plasma after cellulose sulphate treatment. 5. Adrenalectomized rats had significantly increased levels of plasma kininogen, but were normally sensitive to the kininogen-depleting action of cellulose sulphate. 6. The increased plasma kininogen of adrenalectomized rats seems to be a consequence of the impairment of the plasminogen activating mechanism.

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“…A lepirudine-based 30 human whole blood model was used as an inflammation predictor by measuring complement and leuko- 31 cyte stimulation. Alginate microbeads were complement-compatible since they did not activate comple- 32 ment as measured by the soluble terminal complement complex (sTCC), Bb or the anaphylatoxins C3a 33 and C5a. In addition, alginate microbeads were free of surface adherent leukocytes.…”

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confidence: 99%