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MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID
Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular...
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
1966
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2138250/ https://www.ncbi.nlm.nih.gov/pubmed/4958757 |
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author | Blanden, R. V. Mackaness, G. B. Collins, F. M. |
author_facet | Blanden, R. V. Mackaness, G. B. Collins, F. M. |
author_sort | Blanden, R. V. |
collection | PubMed |
description | Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular S. typhimurium pretreated with immune serum, cells from infected animals killed virtually all ingested organisms and did so at an accelerated rate. Macrophages from Listeria monocytogenes-infected mice were shown to possess similarly enhanced microbicidal activity against S. typhimurium. Furthermore, the growth of S. typhimurium in the liver and spleen was more effectively restricted in Listeria-infected mice than in animals vaccinated with heat-killed S. typhimurium, even though the Listeria-infected animals possessed no demonstrable cross-reacting antibody to S. typhimurium. The lack of resistance in the mice vaccinated with heat-killed organisms could not be attributed to any deficiency of humoral factors, since the serum from these animals was as effective at promoting phagocytosis and killing by macrophages as serum from actively infected (and demonstrably resistant) mice. Conversely, Salmonella-infected mice were totally resistant to intravenous challenge with L. monocytogenes. The level of resistance in individual animals was related to the numbers of residual Salmonellae remaining in the tissues; mice with heavier residual infections being the more resistant. Specific antiserum from mice vaccinated with heat-killed S. typhimurium was found to be significantly protective only when the intraperitoneal route of challenge was employed. The foregoing studies have been interpreted to mean that enhancement of the microbicidal ability of macrophages is the mechanism of major importance in acquired resistance to S. typhimurium infection in mice. |
format | Text |
id | pubmed-2138250 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1966 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21382502008-04-17 MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID Blanden, R. V. Mackaness, G. B. Collins, F. M. J Exp Med Article Experiments in vitro comparing normal mouse peritoneal macrophages with cells from Salmonella typhimurium-infected mice have shown that the "immune" macrophages have conspicuously enhanced microbicidal properties. Whereas normal macrophages could inactivate only 50 to 60% of intracellular S. typhimurium pretreated with immune serum, cells from infected animals killed virtually all ingested organisms and did so at an accelerated rate. Macrophages from Listeria monocytogenes-infected mice were shown to possess similarly enhanced microbicidal activity against S. typhimurium. Furthermore, the growth of S. typhimurium in the liver and spleen was more effectively restricted in Listeria-infected mice than in animals vaccinated with heat-killed S. typhimurium, even though the Listeria-infected animals possessed no demonstrable cross-reacting antibody to S. typhimurium. The lack of resistance in the mice vaccinated with heat-killed organisms could not be attributed to any deficiency of humoral factors, since the serum from these animals was as effective at promoting phagocytosis and killing by macrophages as serum from actively infected (and demonstrably resistant) mice. Conversely, Salmonella-infected mice were totally resistant to intravenous challenge with L. monocytogenes. The level of resistance in individual animals was related to the numbers of residual Salmonellae remaining in the tissues; mice with heavier residual infections being the more resistant. Specific antiserum from mice vaccinated with heat-killed S. typhimurium was found to be significantly protective only when the intraperitoneal route of challenge was employed. The foregoing studies have been interpreted to mean that enhancement of the microbicidal ability of macrophages is the mechanism of major importance in acquired resistance to S. typhimurium infection in mice. The Rockefeller University Press 1966-10-01 /pmc/articles/PMC2138250/ /pubmed/4958757 Text en Copyright © 1966 by The Rockefeller University Press 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 Blanden, R. V. Mackaness, G. B. Collins, F. M. MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title | MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title_full | MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title_fullStr | MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title_full_unstemmed | MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title_short | MECHANISMS OF ACQUIRED RESISTANCE IN MOUSE TYPHOID |
title_sort | mechanisms of acquired resistance in mouse typhoid |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2138250/ https://www.ncbi.nlm.nih.gov/pubmed/4958757 |
work_keys_str_mv | AT blandenrv mechanismsofacquiredresistanceinmousetyphoid AT mackanessgb mechanismsofacquiredresistanceinmousetyphoid AT collinsfm mechanismsofacquiredresistanceinmousetyphoid |