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    Modulatory effects of hen egg-white lysozyme on immune response in mice

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    The effect of her egg-white lysozyme (HEWL) on immune response was evaluated by measuring antibody-producing cells and circulating antibodies in mice inoculated with the test antigen (SRBC or BSA) and HEWL at the same time but in a separate body area. HEWL caused a premature decline in SRBC-specific plaque forming cells (PFC) and a reduction in the total amount of these cells. HEWL inhibited antibody production against BSA in the primary response, but was devoid of any effect on the secondary response elicited in the same mice by a second inoculation of the test antigen. The inhibitory effect of HEWL was dose-dependent, being maximal with 300 micrograms, required an enzymatically active protein and was not shown by other basic proteins. HEWL also abolished the enhancing effect of LPS and CFA on anti-BSA antibody production. The inhibitory activity of HEWL was further increased by hydrolyzed peptidoglycan. These results suggest that HEWL modulates the immune response in mice and performs this function through activation of non-specific suppression mechanisms

    The staphylococcal endo-ß-N-acetyl-glucosaminidase inhibits response of human lymphocytes to mitogens and interferes with production of antibodies in mice.

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    The effect of a bacteriolytic enzyme, the endo-beta-N-acetylglucosaminidase excreted by Staphylococcus aureus (SaG) on the response of human lymphocytes to mitogens and on the immune response in mice has been studied. SaG inhibited incorporation of [3H]thymidine into TCA-precipitable material by human peripheral lymphocytes stimulated either by phytohemagglutinin or by concanavalin A, as well as formation of cytoplasmic immunoglobulin-containing cells by B lymphocytes treated with pokeweed mitogen. In all cases the level of inhibition first increased with the SaG concentrations reaching values of over 80% at an enzyme concentration of 100 micrograms/ml, and then decreased. Heat-inactivated SaG as well as SaG treated with both polyclonal and monoclonal specific antibodies or enzyme inhibitors such as chitotriose or hydrolyzed peptidoglycan had no effect on lymphocyte response to mitogens. In mice, SaG at a dose of 300 micrograms per mouse was found to cause a fourfold decrease in the anti-BSA antibody titer and an approximately 70-75% reduction in the immunoglobulin-containing cells in the spleens of mice injected with sheep red blood cells. SaG also completely abolished the enhancing effect of adjuvants such as muramyldipeptide, Freund's complete adjuvant, and Escherichia coli lipopolysaccharide. When SaG was injected into mice together with S. aureus peptidoglycan hydrolyzed either by SaG or by human lysozyme, the inhibitory effect on both production of anti-BSA circulating antibodies and appearance of Igc cells in the spleens of mice injected with sheep red blood cells was enhanced. As we know that (a) human tissues contain endo-beta-N-acetylglucosaminidases; (b) other human hexosaminidases (lysozymes) have previously been shown to interfere with the functions of immunocompetent cells; and (c) products of hexosaminidase hydrolysis of peptidoglycan (muropeptides) known to modulate immune response are ordinarily found in the urine of healthy persons, the possibility that hexosaminidases play a major role in the regulation of the immune response is raised and discussed

    Lysozyme inhibitors enhance immune response in mice.

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    The effect of hen egg-white lysozyme (HEWL) inhibitors (such as heparin, histidine methylester, chitotriose, chitobiose) on immune response was evaluated by measuring antibody-producing cells and circulating antibodies in mice inoculated with these substances and the test antigen (SRBC or BSA). It was found that these compounds have an immuno-enhancing effect which is directly proportional to their inhibitory activity on HEWL. Conversely, HEWL inhibited the immunoenhancing effect of these compounds when injected together with these and the test antigen. The results suggest that one possible mechanism by which adjuvants stimulate immune response may be the inhibition of endogenous lysozyme

    Preliminary characterization of a mutant of herpes simplex virus type 1 selected for acycloguanosine resistance in vitro

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    In this paper we report on the preliminary characterization of a mutant of herpes simplex virus type 1 (HSV‐1) selected for acycloguanosine (acyclovir, ACV) resistance in vitro. The ACVr virus was examined for a series of parameters that include chemosensitivity assay, thymidine kinase (TK) activity, in vitro and in vivo growth, and mutation mapping. The data obtained indicate that a mutated TK gene is responsible for the ACVr phenotype. A distinctive feature of this mutant is the high level of resistance exhibited to ACV (100 μM) and the concomitant presence of a functional TK activity. Such a property makes this virus useful as a model for the study of viral resistance to nucleoside‐type analogues in HSV. Copyright © 1988 Wiley‐Liss, Inc., A Wiley Compan

    MODULATORY EFFECTS OF HEN EGG-WHITE LYSOZYME ON IMMUNE RESPONSE IN MICE

    No full text
    The effect of her egg-white lysozyme (HEWL) on immune response was evaluated by measuring antibody-producing cells and circulating antibodies in mice inoculated with the test antigen (SRBC or BSA) and HEWL at the same time but in a separate body area. HEWL caused a premature decline in SRBC-specific plaque forming cells (PFC) and a reduction in the total amount of these cells. HEWL inhibited antibody production against BSA in the primary response, but was devoid of any effect on the secondary response elicited in the same mice by a second inoculation of the test antigen. The inhibitory effect of HEWL was dose-dependent, being maximal with 300 micrograms, required an enzymatically active protein and was not shown by other basic proteins. HEWL also abolished the enhancing effect of LPS and CFA on anti-BSA antibody production. The inhibitory activity of HEWL was further increased by hydrolyzed peptidoglycan. These results suggest that HEWL modulates the immune response in mice and performs this function through activation of non-specific suppression mechanism
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