Large amounts of each C'3, C'5, C'6, C'7, C'8, and C'9 were consumed when guinea pig serum was incubated with endotoxic lipopolysaccharide, zymosan, or preformed immune complexes. Since these C' components subserve several of the biological activities which follow the injection of endotoxins into experimental animals, these experiments support the hypothesis that certain biological effects induced by endotoxins may be mediated via the C' system, and may account for some of the known similarity in the reactivities evoked by endotoxins and immune complexes in vivo.
Peritoneal and peripheral blood monocyte-macrophages from inbred Lewis (LEW) rats generate higher levels of reactive oxygen intermediates (ROI) in response to group A streptococcal cell walls (SCW) than do similar populations of cells from histocompatible Fischer rats. This differential sensitivity of the phagocytes to SCW is reflected in differences in susceptibility of the two strains to the development of arthritis in response to SCW. After systemic administration of the SCW, LEW rats develop acute and chronic erosive polyarthritis, whereas the Fischer rats are arthritis resistant. Inasmuch as these data suggested that the SCW-induced release of inflammatory cell products such as ROI might be an important contributory factor in the pathogenesis of arthritis in the LEW rats, the animals were injected with SCW and treated with ROI inhibitors. A single intraarticular injection of superoxide dismutase or catalase significantly reduced the SCW-induced inflammatory response and evolution of erosive arthritis in the treated animals (articular index 3.6 +/- 0.36 for SCW only vs 1.4 +/- 0.3 for SCW + SOD; p less than 0.001; n = 6). These data indicate that ROI play a pivotal role in synovitis and, furthermore, that suppression of these inflammatory mediators modulates both acute and chronic SCW-induced inflammation of the joint.
Actinomyces viscosus , a normal inhabitant of the oral cavity, has previously been shown to evoke immune responses in the host. Macrophage activation by this microorganism was studied in a murine system. Peritoneal macrophages, activated in vivo by A. viscosus had a suppressive effect on lymphocyte proliferation in vitro ; total suppression occurred at a PEC to lymphocyte ratio of 6:10. A. viscosus ‐activated macrophages also suppressed the proliferation of normal syngeneic fibroblasts, with a 96% suppression at a PEC to fibroblast ratio of 9:1. Resident peritoneal macrophages had no suppressive effect on either target cell population. Suppression of fibroblast proliferation by A. viscosus ‐activated macrophages was partially reversed by catalase (20000 U/ml) or indomethacin (10 ‐5 M), suggesting involvement of hydrogen peroxide and cylo‐oxygenase product(s). A. viscosus ‐activated macrophages produced, upon stimulation, large amounts of H 2 O 2 (256 nmole per mg protein, in 120 min) which were comparable to those produced by C. parvum ‐activated macrophages. Resident peritoneal macrophages produced only minor quantities of H 2 O 2 under the same conditions. The suppressive effects observed suggest that A. viscosus , by activating macrophages, may modulate the host's immune response and may hamper the repair potential of chronically inflamed connective tissue by inhibition of fibroblast proliferation. Other constitutents of the plaque may share this effect.
Bacterial lipopolysaccharides (LPS) derived from a variety of organisms effectively induced C consumption in humans, bovines, and porcines with developmental agammaglobulinemia; birds with experimental agammaglobulinemia; and humans with agammaglobulinemia syndromes. This interaction proceeded even in precolostral piglet sera which contained less than 2.5 x 10(-6) mg/ml gamma globulin, and led to generation of neutrophil chemotactic factor and anaphylatoxin in these sera. Hence, the LPS-C interaction can proceed in sera markedly deficient in immunoglobulin. The question of whether immunoglobulins can be bypassed in the LPS-C interaction, or whether they are regularly utilized in a way so efficient that their participation is masked, was considered.
Research Articles| July 21 2009 The Complement Profile in Acute Glomerulonephritis Systemic Lupus erythematosus and Hypocomplementemic Chronic Glomerulonephritis: Contrasts and Experimental Correlations Subject Area: Immunology and Allergy H. Gewurz; H. Gewurz The Pediatric Research Laboratories of the Variety Club Heart Hospital and the Department of Microbiology of the University of Minnesota, Minneapolis, Minn., and the Immunology Section, Laboratory of Microbiology, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Search for other works by this author on: This Site PubMed Google Scholar R.J. Pickering; R.J. Pickering The Pediatric Research Laboratories of the Variety Club Heart Hospital and the Department of Microbiology of the University of Minnesota, Minneapolis, Minn., and the Immunology Section, Laboratory of Microbiology, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Search for other works by this author on: This Site PubMed Google Scholar S.E. Mergenhagen; S.E. Mergenhagen The Pediatric Research Laboratories of the Variety Club Heart Hospital and the Department of Microbiology of the University of Minnesota, Minneapolis, Minn., and the Immunology Section, Laboratory of Microbiology, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Search for other works by this author on: This Site PubMed Google Scholar R.A. Good R.A. Good The Pediatric Research Laboratories of the Variety Club Heart Hospital and the Department of Microbiology of the University of Minnesota, Minneapolis, Minn., and the Immunology Section, Laboratory of Microbiology, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Search for other works by this author on: This Site PubMed Google Scholar International Archives of Allergy and Applied Immunology (1968) 34 (6): 556–570. https://doi.org/10.1159/000230149 Article history Published Online: July 21 2009 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation H. Gewurz, R.J. Pickering, S.E. Mergenhagen, R.A. Good; The Complement Profile in Acute Glomerulonephritis Systemic Lupus erythematosus and Hypocomplementemic Chronic Glomerulonephritis: Contrasts and Experimental Correlations. International Archives of Allergy and Applied Immunology 1 June 1968; 34 (6): 556–570. https://doi.org/10.1159/000230149 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsInternational Archives of Allergy and Applied Immunology Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1968Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.
Histamine release from washed peripheral blood basophils of thirty-three subjects with varying degrees of periodontal disease was studied. Dental plaque, serum and basophil leucocytes were collected from individual patients. There was no histamine release when autologous, washed sonicated plaque was added to leucocytes. However, the incubation of autologous plaque with serum at 37 degrees C for 30 min generated a factor which induced histamine release from basophils. This serum factor was stable to heat (56 degrees C, 30 min), eluted from a Sephadex G-100 column at a volume corresponding to a molecular weight of approximately 16,000 daltons and its action was inhibited by antibody to C5. This factor, therefore, is probably C5a. There was a variation in the degree of histamine release seen with the leucocytes of different donors. This variability was a property of the basophil rather than a function of the serum. Basophils from patients with gingival indices of 0.5 to 1.0 had significantly more histamine release than basophils from patients with gingival indices of less than 0.5 or greater than 1.5 (P less than 0.001). These experiments demonstrate that dental plaque activates serum to form C5a which in turn releases histamine from basophils. However, these experiments do not indicate a role for IgE in this reaction since the direct interaction of plaque with basophils did not cause histamine release. The release of mediators from mast cells could play an important role in the induction of the inflammatory response in periodontal disease.
