Abstract
Bovine serum albumin (BSA) in complete Freund's adjuvant (CFA) was injected into the knee joints of previously BSA-sensitized guinea pigs and rabbits. The primary immune reaction to BSA prevented secondary immune response toTrichinella larvae infection. We were unable to produce either eosinophilia in the peripheral blood or antibodies againstTrichinella antigen (shown by complement fixation test). The additional injection of mediators of the inflammatory reaction or their precursors, e.g., complement component C5 and arachidonic acid, caused different histological pictures. C5 produced a prolonged acute inflammatory phase with abundant neutrophils, whereas arachidonic acid did not significantly change the inflammatory response as compared to controls. The additional application of eosinophil-enriched preparation (EEP) caused a conspicuously reduced influx of monocytes/macrophages, a reduction of lymphocyte numbers, a prolonged influx of neutrophils, increased arylsulfatase activity, earlier reduction of the inflammatory process, and earlier onset of synoviocyte regeneration as compared to controls.
Similar content being viewed by others
References
Ehrlich, P. 1879. über die spezielle Granulation des Blutes.Arch. Anat. Physiol. p. 571; Verh. der physiol. Ges. zu Berlin, 17. Sitzung, 20. Juni 1879.
Anderson, W. A. D. 1971. Pathology, Vol. 1, 6th ed. C. V. Mosby, St. Louis, 735–737.
Soren, A. 1978. Histodiagnosis and Clinical Correlation of Rheumatoid and Other Synovitis. G. Thieme, Stuttgart. 43–57.
Popper, H., Picher, O., andAuer, H. 1982. Reduction of carrageenan-, bradykinin-, and histamine-induced acute inflammation by experimental eosinphilia in rats.Immunology 46:589–594.
Weller. P. F., andGoetzl, E. J. 1980. The human eosinophil: Roles in host defense and tissue injury.Am. J. Pathol. 100:791–820.
Zeiger, R. R., Yurding, D. L., andColten, H. R. 1976. Histamine metabolism. II Cellular and subcellular localisation of the catabolic enzymes, histaminase and histamine methyltransferase in human leukocytes.J. Allergy Clin. Immunol. 58:172–179.
Wassermann, S. I., Goetzl, E. J., andAusten, K. F. 1975. Inactivation of slow reacting substance of naphylaxis by human eosinophil arylsulfatase.J. Immunol. 114:645–649.
Kater, L. A., Goetzl, E. J., andAusten, K. F. 1976. Isolation of human eosinophil phospholipase D.J. Clin. Invest. 57:1173–1180.
Berenberg, J. A., andWard, P. A. 1973. Chemotactic factor inactivator in normal human serum.J. Clin. Invest. 52:1200.
Weller, P. F., Goetzl, E. J., andAusten, K. F. 1980. Identification of human eosinophil lysophospholipase as the constituent of Charcot-Leyden crystals.Proc. Natl. Acad. Sci. U.S.A. 77:7440–7443.
Bass, D. A. 1975. Behaviour of eosinophil leukocytes in acute inflammation: II Eosinophil dynamics during acute inflammation.J. Clin. Invest. 56:870–879.
Bass, D. A., Gonwa, Th. A., Szejda, P., Consart, M. S., Dechatelet, L. R., andMcCall, C. E., 1980. Eosinophenia of acute infection: Production of eosinopenia by chernotactic factors of acute inflammation.J. Clin: Invest. 65:1265–1271.
Bass, D. A. 1977. Reproduction of the eosinopenia of acute infection by passive transfer of a material obtained from inflammatory exsudate.Infect. Immun. 15:410–416.
Gartner, I. 1980. Separation of human eosinophils in density gradients of polyvinylpyrrolidone-coated silica gel.Immunology 40:133–136.
Pearse, A. E. G. 1968. Histochemistry, Vol. 2, 3rd ed. J and A. Churchill, London. 1303–1304, 1322, 1363.
Tice, L. W., andWollman, S. H. 1972. Ultrastructural localisation of peroxidase activity on some membranes of the typical thyroid epithelial cell.Lab. Invest. 26:63.
Sternberg, L. 1979. Immunocytochemistry, 2nd ed. J. Wiley, New York.
MØller-Graabaek, P. 1982. Ultrastructural evidence for two distinct types of synoviocytes in rat synovial membrane.J. Ultrastruct. Res. 78:321–339.
Van Den Berg, W. B., Haasakker, T. E., Bax, J., andScheper, R. J. 1980. Suppression of antibody-mediated accumulation of eosinophils in chronic inflammatory lesions by concomitant delayed hypersensitivity reactions.Immunology 41:981–988.
Kownatzki, E., andTill, G. 1977. The effect of histamine on chemotactic migration of eosinophil granulocytes towards complement derived chemotactic factors.Allergol. Immunopathol. 5:296.
Nathan, C. F., Karnofsky, M. L., andDavid, J. R. 1971. Alterations of macrophage functions by mediators from lymphocytes.J. Exp. Med. 133:1356.
Frigas, E., Loegering, D. A., andErlich, G. J. 1980. Cytotoxic effects of the guinea pig eosinophil major basic protein on tracheal epithelium.Lab. Invest. 42:35–43.
Henderson, W. R., Chi, E. Y., Jong, E. C., andKlebanoff, S. J. 1981. Mast cell-mediated tumor-cell cytotoxicity. Role of the peroxidase system.J. Exp. Med. 153:520–533.
Ogawa, H., Kunkel, St. L., Fantone, J. C., andWard, P. A. 1981. Digestion of the fifth component of complement by eosinophil lysosomal enzymes.Virchows Arch. B. 38:149–157.
Wasserman, S. L. Goetzl, E. J., andAusten, K. F. 1975. Inactivation of slow reacting substance of anaphylaxis by human eosinophil arylsulfatase.J. Immunol. 114:645–649.
Author information
Authors and Affiliations
Additional information
Parts of this work were presented as a poster at the 5th European Immunology Meeting, June 1–4, 1982, in Istanbul.
Rights and permissions
About this article
Cite this article
Popper, H. Experimental monoarthritis. Inflammation 8, 301–312 (1984). https://doi.org/10.1007/BF00916418
Issue Date:
DOI: https://doi.org/10.1007/BF00916418