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Studies on glycogen-induced inflammation of mice

Dynamics of inflammatory responses and influence of antiinflammatory drugs and protease inhibitors

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Abstract

The intraperitoneal injection of glycogen in the mouse resulted, shortly thereafter, in the accumulation of 14–23 million neutrophils in the peritoneal cavity and a four-fold increase in the numbers of circulating neutrophils. Preceding the influx of leukocytes, the exudation of plasma proteins and the chemotactic activity for mouse neutrophil in vitro increased in the peritoneal fluid. Among various protease inhibitors examined, chymostatin alone suppressed the plasma protein exudation. Indomethacin and dexamethasone reduced the accumulation of white cells and protein exudation. These nonsteroidal and steroidal antiinflammatory drugs were equally effective whether given simultaneously with or 60 min before glycogen or whether administered intraperitoneally or orally. Colchicine showed a suppressive effect on the leukocyte accumulation but enhanced the protein exudation.

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References

  1. Hirsch, J. G., andA. B. Church. 1960. Studies of phagocytosis of group A streptococci by polymorphonuclear leukocytes in vitro.J. Exp. Med. 111:309–322.

    Google Scholar 

  2. Hirsch, J. G. 1960. Further studies on preparation and properties of phagocytin.J. Exp. Med 111:323–337.

    Google Scholar 

  3. Yamashita, T., N. Imaizumi, andS. Yuasa. 1979. Effect of endocellular cryoprotectant upon polymorphonuclear neutrophil function during storage at low temperature.Cryobiology 16:112–117.

    Google Scholar 

  4. Yamashita, T., K. Takamori, andY. Tanaka. 1979. A possible preferential inhibition of chemotaxis of polymorphonuclear neutrophils by a chemical modification.Experientia 35:1345–1347.

    Google Scholar 

  5. Yamashita, T., Y. Tanaka, andH. Matsuzawa. 1980. Cytoplasmic and plasma membrane adenosine triphosphatase of polymorphonuclear neutrophils. Comparison of their enzymatic properties and attempt for a direct determination of myosin ATPase activity using polymorphonuclear neutrophil extract.Biochim. Biophys. Acta 599:246–253.

    Google Scholar 

  6. Ishibashi, Y., andT. Yamashita. 1981. Generation of a phagocytosis-stimulating factor by polymorphonuclear neutrophils during phagocytosis.Int. Arch. Allergy Appl. Immunol. 64:181–189.

    Google Scholar 

  7. Nagaoka, I., andT. Yamashita. 1981. Inactivation of phagocytosis-stimulating activity of tuftsin by polymorphonuclear neutrophils. A possible role of leucine aminopeptidase as an ecto-enzyme.Biochim. Biophys. Acta 675:85–93.

    Google Scholar 

  8. Snyderman, R., J. K. Phillips, andS. E. Mergenhagen. 1971. Biological activity of complement in vivo. Role of C5 in the accumulation of polymorphonuclear leukocytes in inflammatory exudates.J. Exp. Med. 134:1131–1143.

    Google Scholar 

  9. Weichselbaum, T. E. 1946. Accurate and rapid method for the determination of proteins in small amounts of blood serum and plasma.Am. J. Clin. Pathol. Tech. Sect. 10:40–49.

    Google Scholar 

  10. Yamashita, T. 1959. Studies on muscle glycogen (I). About the fractions of muscle glycogen of frog.Seikagaku 31:300–309 (in Japanese).

    Google Scholar 

  11. Whittle, B. A. 1964. The use of changes in capillary permeability in mice to distinguish between narcotic and nonnarcotic analgesics.Br. J. Pharmacol. 22:246–253.

    Google Scholar 

  12. Hayashi, H. 1975. The intracellular neutral SH-dependent protease associated with inflammatory reactions.Int. Rev. Cytol. 40:101–151.

    Google Scholar 

  13. Movat, H. Z. 1979. Kinins and kinin system as inflammatory mediators.In Chemical Messengers of the Inflammatory Process. J. C. Houck, editor. Elsevier/North-Holland Biomedical Press, Amsterdam. 47–112.

    Google Scholar 

  14. Gleisner, J. M. 1979. Lysosomal factors in inflammation.In Chemical Messengers of the Inflammatory Process. J. C. Houck, editor. Elsevier/North-Holland Biomedical Press, Amsterdam. 229–260.

    Google Scholar 

  15. Moncada, S., S. H. Ferreira, andJ. R. Vane. 1973. Prostaglandins, aspirin-like drugs and the oedema of inflammation.Nature 246:217–219.

    Google Scholar 

  16. Lewis, A. J., D. J. Nelson, andM. F. Sugrue. 1975. On the ability of prostaglandin Ei and arachidonic acid to modulate experimentally induced oedema in the rat paw.Br. J. Pharmacol. 55:51–56.

    Google Scholar 

  17. Williams, T. J., andJ. Morley. 1973. Prostaglandins as potentiators of increased vascular permeability in inflammation.Nature 246:215–217.

    Google Scholar 

  18. Thomas, G., andG. B. West. 1973. Prostaglandins as regulators of bradykinin responses.J. Pharm. Pharmacol. 25:747–748.

    Google Scholar 

  19. Ferreira, S. H. 1979. Prostaglandins.In Chemical Messengers of the Inflammatory Process. J. C. Houck, editor. Elsevier/North-Holland Biomedical Press, Amsterdam. 113–151.

    Google Scholar 

  20. Turner, S. R., J. A. Trainer, andW. S. Lynn. 1975. Biogenesis of chemotactic molecules by the arachidonate lipoxygenase system of platelets.Nature 257:680–681.

    Google Scholar 

  21. Goetzl, E. J., J. M. Woods, andR. R. Gorman. 1977. Stimulation of human eosinophil and neutrophil polymorphonuclear leukocyte chemotaxis and random migration by 12-Lhydroxy-5, 8, 10, 14-eicosatetraenoic acid.J. Clin. Invest. 59:179–183.

    Google Scholar 

  22. Malmsten, C. L., J. Palmblad, A.-M. Udèn, O. Rådmark, L. Engstedt, andB. Samuelsson. 1980. Leukotriene B4: A highly potent and stereospecific factor stimulating migration of polymorphonuclear leukocytes.Acta Physiol. Scand. 110:449–451.

    Google Scholar 

  23. Goetzl, E. J., andW. C. Pickett. 1980. The human PMN leukocyte chemotactic activity of complex hydroxy-eicosatetraenoic acids (HETEs).J. Immunol. 125:1789–1791.

    Google Scholar 

  24. Smith, M. J. H., A. W. Ford-Hutchinson, andM. A. Bray. 1980. LeukotrieneB: A potential mediator of inflammation.J. Pharm. Pharmacol. 32:517–518.

    Google Scholar 

  25. Ford-Hutchinson, A. W., M. A. Bray, M. V. Doig, M. E. Shipley, andM. J. H. Smith. 1980. Leukotriene B, a potent chemokinetic and aggregating substance released from polymorphonuclear leukocytes.Nature 286:264–265.

    Google Scholar 

  26. Goetzl, E. J., A. R. Brash, A. I. Tauber, J. A. Oates, andW. C. Hubbard. 1980. Modulation of human neutrophil function by monohydroxy-eicosatetraenoic acids.Immunology 39:491–501.

    Google Scholar 

  27. Vane, J. R. 1971. Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.Nature (London)New Biol. 231:232–235.

    Google Scholar 

  28. Smith, J. B., andA. L. Willis. 1971. Aspirin selectively inhibits prostaglandin production in human platelets.Nature (London),New Biol. 231:235–237.

    Google Scholar 

  29. Ferreira, S. H., S. Moncada, andJ. R. Vane. 1971. Indomethacin and aspirin abolish prostaglandin release from the spleen.Nature (London),New Biol. 231:237–239.

    Google Scholar 

  30. Ferreira, S. H., andJ. R. Vane. 1974. New aspects of the mode of action of nonsteroid antiinflammatory drugs.Annu. Rev. Pharmacol. 14:57–73.

    Google Scholar 

  31. Flower, R. J. 1974. Drugs which inhibit prostaglandin biosynthesis.Pharmacol. Rev. 26:33–67.

    Google Scholar 

  32. Hamberg, M., J. Svensson, andB. Samuelsson. 1974. Prostaglandin endoperoxides. A new concept concerning the mode of action and release of prostaglandins.Proc. Natl. Acad. Sci. U.S.A. 71:3824–3828.

    Google Scholar 

  33. Hamberg, M., andB. Samuelsson. 1974. Prostaglandin endoperoxide. Novel transformations of arachidonic acid in human platelets.Proc. Natl. Acad. Sci. U.S.A. 71:3400–3404.

    Google Scholar 

  34. Roth, G. J., N. Stanford, andP. W. Majerus. 1975. Acetylation of prostaglandin synthetase by aspirin.Proc. Natl. Acad. Sci. U.S.A. 72:3073–3076.

    Google Scholar 

  35. Rome, L. H., W. E. Lands, G. J. Roth, andP. W. Majerus. 1976. Aspirin as a quantitative acetylating reagent for the fatty acid oxygenase that forms prostaglandins.Prostaglandins 11:23–30.

    Google Scholar 

  36. Gryglewski, R. J., B. Panczenko, R. Korbut, L. Grodzinska, andA. Ocetkiewicz. 1975. Corticosteroids inhibit prostaglandin release from perfused mesenteric blood vessels of rabbit and from perfused lungs of sensitized guinea pig.Prostaglandins 10:343–355.

    Google Scholar 

  37. Lewis, G. P., andP. J. Piper. 1975. Inhibition of release of prostaglandins as an explanation of some of the actions of antiinflammatory corticosteroids.Nature 254:308–311.

    Google Scholar 

  38. Kantrowitz, F., D. R. Robinson, andM. B. McGuire. 1975. Corticosteroids inhibit prostaglandin production by rheumatoid synovia.Nature 258:737–739.

    Google Scholar 

  39. Tashjian, A. H., Jr., E. F. Voelkel, J. McDonough, andL. Levine. 1975. Hydrocortisone inhibits prostaglandin production by mouse fibrosarcoma cells.Nature 258:739–741.

    Google Scholar 

  40. Floman, Y., andU. Zor. 1976. Mechanism of steroid action in inflammation: Inhibition of prostaglandin synthesis and release.Prostaglandins 12:403–413.

    Google Scholar 

  41. Nijkamp, F. P., R. J. Flower, S. Moncada, andJ. R. Vane. 1976. Partial purification of rabbit aorta contracting substance-releasing factor and inhibition of its activity by antiinflammatory steroids.Nature 263:479–482.

    Google Scholar 

  42. Hong, S.-C. L., andL. Levine. 1976. Inhibition of arachidonic acid release from cells as the biochemical action of antiinflammatory corticosteroids.Proc. Natl. Acad. Sci. U.S.A. 73:1730–1734.

    Google Scholar 

  43. Blackwell, G. J., R. J. Flower, F. P. Nijkamp, andJ. R. Vane. 1978. Phospholipase A2 activity of guinea-pig isolated perfused lungs: stimulation and inhibition by antiinflammatory steroids.Br. J. Pharmacol. 62:79–89.

    Google Scholar 

  44. Tam, S., S.-C. L. Hong, andL. Levine. 1977. Relationships, among the steroids, of antiinflammatory properties and inhibition of prostaglandin production and arachidonic acid release by transformed mouse fibroblasts.J. Pharmac. Exp. Ther. 203:162–168.

    Google Scholar 

  45. Danon, A., andG. Assouline. 1978. Inhibition of prostaglandin biosynthesis by corticosteroids requires RNA and protein synthesis.Nature 273:552–554.

    Google Scholar 

  46. Flower, R. J., andG. J. Blackwell. 1979. Antiinflammatory steroids induce biosynthesis of a phospholipase A2 inhibitor which prevents prostaglandin generation.Nature 278:456–459.

    Google Scholar 

  47. DiRosa, M., andP. Persico. 1979. Mechanism of inhibition of prostaglandin biosynthesis by hydrocortisone in rat leukocytes.Br. J. Pharmacol. 66:161–163.

    Google Scholar 

  48. Carnuccio, R., M. Dirosa, andP. Persico. 1980. Hydrocortisone-induced inhibitor of prostaglandin biosynthesis in rat leukocytes.Br. J. Pharmacol. 68:14–16.

    Google Scholar 

  49. Tsurufuji, S., K. Sugio, andF. Takemasa. 1979. The role of glucocorticoid receptor and gene expression in the antiinflammatory action of dexamethasone.Nature 280:408–410.

    Google Scholar 

  50. Borel, J. F. 1973. Effect of some drugs on the chemotaxis of rabbit neutrophils in vitro.Experientia 29:676–678.

    Google Scholar 

  51. Rivkin, I., G. V. Foschi, andC. H. Rosen. 1976. Inhibition of in vitro neutrophil chemotaxis and spontaneous motility by antiinflammatory agents.Proc. Soc. Exp. Biol. Med. 153:236–240.

    Google Scholar 

  52. Caner, J. E. Z. 1965. Colchicine inhibition of chemotaxis.Arthritis Rheum. 8:757–760.

    Google Scholar 

  53. Ward, P. A. 1971. Leukotactic factors in health and disease.Am. J. Pathol. 64:521–530.

    Google Scholar 

  54. Bandmann, U., L. Rydgren, andB. Norberg. 1974. The difference between random movement and chemotaxis. Effects of antitubulins on neutrophil granulocyte locomotion.Exp. Cell Res. 88:63–73.

    Google Scholar 

  55. Ramsey, W. S., andA. Harris. 1973. Leucocyte locomotion and its inhibition by antimitotic drugs.Exp. Cell Res. 82:262–270.

    Google Scholar 

  56. Becker, E. L., andH. J. Showell. 1974. The ability of chemotactic factors to induce lysosomal enzyme release. II. The mechanism of release.J. Immunol. 112:2055–2062.

    Google Scholar 

  57. Dinarello, C. A., M. J. Chusid, A. S. Fauci, J. I. Gallin, D. C. Dale, andS. M. Wolff. 1976. Effect of prophylactic colchicine therapy on leukocyte function in patients with familial Mediterranean fever.Arthritis Rheum. 19:618–622.

    Google Scholar 

  58. Borisy, G. G., andE. W. Taylor. 1967. The mechanism of action of colchicine. Binding of colchicine-3H to cellular protein.J. Cell Biol. 34:525–533.

    Google Scholar 

  59. Borisy, G. G., andE. W. Taylor. 1967. The mechanism of action of colchicine. Colchicine binding to sea urchin eggs and the mitotic apparatus.J. Cell Biol. 34:535–548.

    Google Scholar 

  60. Malawista, S. E., andK. G. Bensch. 1967. Human polymorphonuclear leukocytes: Demonstration of microtubules and effect of colchicine.Science 156:521–522.

    Google Scholar 

  61. Robinson, D. R., andL. Levine. 1974. Prostaglandin concentrations in synovial fluid in rheumatic diseases: Action of indomethacin and aspirin.In Prostaglandin Synthetase Inhibitors. H. J. Robinson and J. R. Vane, editors. Raven Press, New York. 223–228.

    Google Scholar 

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Yamashita, T., Ishibashi, Y., Nagaoka, I. et al. Studies on glycogen-induced inflammation of mice. Inflammation 6, 87–101 (1982). https://doi.org/10.1007/BF00910722

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