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Humoral mediated macrophage response during tumour growth.
Reticuloendothelial (RE) phagocytic and circulating plasma opsonic activity was evaluated in rats transplanted with the Walker 256 carcinoma tumour in an attempt to evaluate the role of opsonic protein in governing the functional state of the macrophage system. Animals transplanted intramuscularly w...
Autores principales: | , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
1975
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2024772/ https://www.ncbi.nlm.nih.gov/pubmed/1212411 |
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author | Saba, T. M. Antikatzides, T. G. |
author_facet | Saba, T. M. Antikatzides, T. G. |
author_sort | Saba, T. M. |
collection | PubMed |
description | Reticuloendothelial (RE) phagocytic and circulating plasma opsonic activity was evaluated in rats transplanted with the Walker 256 carcinoma tumour in an attempt to evaluate the role of opsonic protein in governing the functional state of the macrophage system. Animals transplanted intramuscularly with 2 X 10(4) viable tumour cells manifested 2 peaks of RE stimulation at 6 and 14 days post-transplantation with a subsequent decline in the phagocytic activity over the 14-30 day period. Increased phagocytic activity as determined by colloid clearance was primarily a reflection of hepatic Küpffer cell hyperphagocytosis while the decline in phagocytic activity was related to a decrease in Küpffer cell function. The initial peak of RE stimulation was associated with an elevation in the blood opsonin level and no significant enlargement of the liver and spleen. In contrast, the second peak of RE stimulation at 14 days was associated with both an elevation in opsonin levels and an associated hepatic and splenic enlargement. The decline in phagocytic activity over the 14-30 day interval was associated with a progressive decline in the plasma opsonic activity, a return of the spleen to its normal size in relationship to the body weight, and a persistent hepatomegaly. These findings suggest that the alterations in macrophage function during tumour growth may be mediated in part by changes in the opsonic or phagocytosis promoting capacity of plasma. Since opsonic protein contributes to the discriminatory capacity of macrophages, it is suggested that changes in the blood opsonin level may condition the anti-tumour capacity of the macrophage system with respect to host defence aginst malignant disease. |
format | Text |
id | pubmed-2024772 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1975 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-20247722009-09-10 Humoral mediated macrophage response during tumour growth. Saba, T. M. Antikatzides, T. G. Br J Cancer Research Article Reticuloendothelial (RE) phagocytic and circulating plasma opsonic activity was evaluated in rats transplanted with the Walker 256 carcinoma tumour in an attempt to evaluate the role of opsonic protein in governing the functional state of the macrophage system. Animals transplanted intramuscularly with 2 X 10(4) viable tumour cells manifested 2 peaks of RE stimulation at 6 and 14 days post-transplantation with a subsequent decline in the phagocytic activity over the 14-30 day period. Increased phagocytic activity as determined by colloid clearance was primarily a reflection of hepatic Küpffer cell hyperphagocytosis while the decline in phagocytic activity was related to a decrease in Küpffer cell function. The initial peak of RE stimulation was associated with an elevation in the blood opsonin level and no significant enlargement of the liver and spleen. In contrast, the second peak of RE stimulation at 14 days was associated with both an elevation in opsonin levels and an associated hepatic and splenic enlargement. The decline in phagocytic activity over the 14-30 day interval was associated with a progressive decline in the plasma opsonic activity, a return of the spleen to its normal size in relationship to the body weight, and a persistent hepatomegaly. These findings suggest that the alterations in macrophage function during tumour growth may be mediated in part by changes in the opsonic or phagocytosis promoting capacity of plasma. Since opsonic protein contributes to the discriminatory capacity of macrophages, it is suggested that changes in the blood opsonin level may condition the anti-tumour capacity of the macrophage system with respect to host defence aginst malignant disease. Nature Publishing Group 1975-10 /pmc/articles/PMC2024772/ /pubmed/1212411 Text en https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Article Saba, T. M. Antikatzides, T. G. Humoral mediated macrophage response during tumour growth. |
title | Humoral mediated macrophage response during tumour growth. |
title_full | Humoral mediated macrophage response during tumour growth. |
title_fullStr | Humoral mediated macrophage response during tumour growth. |
title_full_unstemmed | Humoral mediated macrophage response during tumour growth. |
title_short | Humoral mediated macrophage response during tumour growth. |
title_sort | humoral mediated macrophage response during tumour growth. |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2024772/ https://www.ncbi.nlm.nih.gov/pubmed/1212411 |
work_keys_str_mv | AT sabatm humoralmediatedmacrophageresponseduringtumourgrowth AT antikatzidestg humoralmediatedmacrophageresponseduringtumourgrowth |