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Augmentation of metastasis formation by thioglycollate‐elicited macrophages
Author(s) -
Gorelik E.,
Wiltrout R. H.,
Brunda M. J.,
Holden H. T.,
Herberman R. B.
Publication year - 1982
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910290514
Subject(s) - mastocytoma , macrophage , lewis lung carcinoma , metastasis , splenocyte , percoll , lung , cell culture , cell , pathology , cancer research , melanoma , biology , immunology , medicine , spleen , cancer , in vitro , tumor cells , biochemistry , genetics
Inoculation of thioglycollate‐elicited peritoneal exudate cells (PEC) into C57BL/6 mice reduced the rate of lung clearance of several intravenously (i.v.) injected murine tumor cells, and increased by up to 100‐fold the number of artificially‐induced metastatic lung nodules produced by the i.v. injection of B16 melanoma or Lewis lung carcinoma (3LL) tumor cells. Maximum effects were observed when PEC were injected either before, or shortly after, tumor cells. Modulation of lung clearance or metastasis formation was observed only with PEC and not with a variety of other cells, such as splenocytes, thymocytes, P815 mastocytoma cells, or several macrophage‐like cell lines (PU5‐1.8 and IC‐21). Lysates of PEC were as efficient in reducing lung clearance and augmenting metastasis formation as were intact viable PEC. Lysates of other cell types, including P815 and the macrophage‐like cell lines, were unable to produce these effects. PEC populations, enriched for macrophages by adherence to plastic or by percoll density gradient sedimentation, also increased the number of B16‐induced artificial metastasis, implicating the macrophage as the cell responsible for these observations.