Mitogenic activities of synthetic lipid A analogs and suppression of mitogenicity of lipid A

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Published inInfection and Immunity Vol. 44; no. 2; pp. 427 - 433
Main Authors TANAMOTO, K, GALANOS, C, LUDERITZ, O, KUSUMOTO, S, SHIBA, T
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.05.1984
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Abstract Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue Spotlights in the Current Issue IAI About IAI Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy Connect to IAI IAI RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0019-9567 Online ISSN: 1098-5522 Copyright © 2014 by the American Society for Microbiology.   For an alternate route to IAI .asm.org, visit: IAI       
AbstractList The effect of synthetic lipid A analogs on murine spleen cells was studied. The preparations represented D-glucosamine and D-glucosaminyl-beta 1,6-D-glucosamine disaccharide derivatives substituted in different combinations by ester- and amide-bound fatty acids and by phosphate groups. Significant mitogenic activity was demonstrated with a number of synthetic disaccharide preparations; however, their potency was lower than that of lipid A. The synthetic preparations were not mitogenic for spleen cells from C3H/HeJ mice. Furthermore, the mitogenicity of the synthetic preparations was abolished after binding with polymyxin B. The results indicate that for expression of mitogenicity, a phosphate group at position 1 of the reducing glucosamine and amide-bound acyloxyacyl residues are important factors. Some of the synthetic preparations containing the diglucosamine backbone and expressing relatively low mitogenicity suppressed B-cell mitogenicity of lipid A. Although these preparations were lytic for erythrocytes, they did not affect the viability of the splenic lymphocytes. Suppression was seen when the synthetic preparations were added simultaneously with or after the lipid A mitogen, but optimal suppression was expressed when the preparations were added to the system 3 h before lipid A. Washing of the cells before the addition of lipid A did not affect the results. The suppression was not due to the induction of suppressor cells by the synthetic preparations. The disaccharide preparations did not inhibit T-cell mitogenicity of concanavalin A. In contrast to the disaccharide preparations, the monosaccharide preparations suppressed mitogenicity of both lipid A and concanavalin A, probably because of their direct toxicity for lymphocytes.
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Author C Galanos
K Tanamoto
O Lüderitz
S Kusumoto
T Shiba
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Issue 2
Keywords Spleen
Vertebrata
Mammalia
Synthetic product
Structure activity relation
Mouse
Immune stimulation
Analog
Rodentia
B-Lymphocyte
Mitogen
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Snippet Classifications Services IAI Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit...
The effect of synthetic lipid A analogs on murine spleen cells was studied. The preparations represented D-glucosamine and D-glucosaminyl-beta...
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StartPage 427
SubjectTerms Animals
Biological and medical sciences
Cells, Cultured
Fundamental and applied biological sciences. Psychology
Fundamental immunology
Hemolysis - drug effects
Immunobiology
Immunosuppression
Lipid A - analogs & derivatives
Lipid A - chemical synthesis
Lipid A - pharmacology
Lipopolysaccharides - toxicity
Lymphocyte Activation - drug effects
Lymphocytes - drug effects
Lymphocytes - immunology
Mice
Mice, Inbred Strains
Modulation of the immune response (stimulation, suppression)
Polymyxin B - pharmacology
Salmonella - immunology
Sheep
Structure-Activity Relationship
Title Mitogenic activities of synthetic lipid A analogs and suppression of mitogenicity of lipid A
URI http://iai.asm.org/content/44/2/427.abstract
https://www.ncbi.nlm.nih.gov/pubmed/6715043
https://pubmed.ncbi.nlm.nih.gov/PMC263536
Volume 44
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