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INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES

It has been shown that injection of lipopolysaccharides, derived from a variety of Gram-negative bacterial species, evokes in mice a rapidly developing rise in resistance to infection with Gram-negative pathogens. This is accompanied by an elevation in properdin titer, at times to levels 2 to 3 time...

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Autores principales: Landy, Maurice, Pillemer, Louis
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1956
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136568/
https://www.ncbi.nlm.nih.gov/pubmed/13357692
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author Landy, Maurice
Pillemer, Louis
author_facet Landy, Maurice
Pillemer, Louis
author_sort Landy, Maurice
collection PubMed
description It has been shown that injection of lipopolysaccharides, derived from a variety of Gram-negative bacterial species, evokes in mice a rapidly developing rise in resistance to infection with Gram-negative pathogens. This is accompanied by an elevation in properdin titer, at times to levels 2 to 3 times the normal. The rate, magnitude, and duration of these responses are dependent on many factors, the most important of which are the quantity and timing of the lipopolysaccharide administered. The increased resistance to infection evoked in mice by lipopolysaccharides was effective against infections produced by endotoxin-bearing organisms-bacterial species highly susceptible in vitro to the bactericidal action of the properdin system. Properdin titers of mice prior to infection provide an incomplete picture of the subsequent reaction of the host to the infective agent. Following infection with Gram-negative organisms, properdin levels accurately reflect the bacteriologic course and outcome of the infection. Thus, in control animals, properdin titers progressively declined and the animals died, while in mice appropriately treated with lipopolysaccharide, properdin levels were either maintained in the normal range or increased, depending on the dose and time of administration of lipopolysaccharide; this was always accompanied by successful management of the infection. The complex nature of the alterations produced in the host by lipopolysaccharides is stressed. It is pointed out that the increase in the ability of the host to cope with Gram-negative infections may be the result of stimulation of other defense mechanisms, in addition to the properdin system.
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spelling pubmed-21365682008-04-17 INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES Landy, Maurice Pillemer, Louis J Exp Med Article It has been shown that injection of lipopolysaccharides, derived from a variety of Gram-negative bacterial species, evokes in mice a rapidly developing rise in resistance to infection with Gram-negative pathogens. This is accompanied by an elevation in properdin titer, at times to levels 2 to 3 times the normal. The rate, magnitude, and duration of these responses are dependent on many factors, the most important of which are the quantity and timing of the lipopolysaccharide administered. The increased resistance to infection evoked in mice by lipopolysaccharides was effective against infections produced by endotoxin-bearing organisms-bacterial species highly susceptible in vitro to the bactericidal action of the properdin system. Properdin titers of mice prior to infection provide an incomplete picture of the subsequent reaction of the host to the infective agent. Following infection with Gram-negative organisms, properdin levels accurately reflect the bacteriologic course and outcome of the infection. Thus, in control animals, properdin titers progressively declined and the animals died, while in mice appropriately treated with lipopolysaccharide, properdin levels were either maintained in the normal range or increased, depending on the dose and time of administration of lipopolysaccharide; this was always accompanied by successful management of the infection. The complex nature of the alterations produced in the host by lipopolysaccharides is stressed. It is pointed out that the increase in the ability of the host to cope with Gram-negative infections may be the result of stimulation of other defense mechanisms, in addition to the properdin system. The Rockefeller University Press 1956-09-01 /pmc/articles/PMC2136568/ /pubmed/13357692 Text en Copyright © Copyright, 1956, by The Rockefeller Institute for Medical Research New York This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Landy, Maurice
Pillemer, Louis
INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title_full INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title_fullStr INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title_full_unstemmed INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title_short INCREASED RESISTANCE TO INFECTION AND ACCOMPANYING ALTERATION IN PROPERDIN LEVELS FOLLOWING ADMINISTRATION OF BACTERIAL LIPOPOLYSACCHARIDES
title_sort increased resistance to infection and accompanying alteration in properdin levels following administration of bacterial lipopolysaccharides
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136568/
https://www.ncbi.nlm.nih.gov/pubmed/13357692
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