Proliferative capacity of mouse peritoneal macrophages in vitro.

Zeijst, Bernard A.M. van der; Stewart, Carleton C.; Schlesinger, Sondra

doi:10.1084/jem.147.4.1253

Cited by 52 publications

(13 citation statements)

References 25 publications

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“…Thioglycolate-elicited exudate macrophages were able to proliferate and form macrophage colonies in the presence of M-CSF in vitro [12,13]. The macrophage precursors displayed a characteristic lag in initiation of growth compared to the bone marrow macrophage precursors [11]; the lag could be eliminated by the stimulation with GM-CSF [14].…”

Section: Introductionmentioning

confidence: 99%

Macrophage-colony forming cells (M-CFC), with different sensitivities to colony stimulating factors, from peritoneal exudates and tissues of chronically inflamed mice

Müller

Yoshida

1996

Inflamm Res

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Section: Introductionmentioning

confidence: 99%

Macrophage-colony forming cells (M-CFC), with different sensitivities to colony stimulating factors, from peritoneal exudates and tissues of chronically inflamed mice

Müller

Yoshida

1996

Inflamm Res

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“…Normal "resident" macrophages barely proliferate in vitro except when conditioned medium (macrophage growth factor) is added to the cultures of macrophages stimulated with thioglycollate or other stimulants (11,12,34). Using simian virus 40 (SV40) as the growth-stimulating agent, transformed macrophage clones which retain several properties specific to macrophages have been established as proliferating cell lines (13,27).…”

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confidence: 99%

Transformation of Mouse Peritoneal Macrophages and Bone Marrow Cells by Simian Virus 40

Takayama

1980

Microbiology and Immunology

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A fraction of cultured mouse peritoneal macrophages and bone marrow cells acquired the ability to divide after infection by simian virus 40 (SV40). Two types of transformed lines were obtained.Most transformants isolated 40-60 days after infection did not display macrophage specific properties such as ingestion of opsonized red blood cells, possession of Fe receptors and complement receptors, and acid phosphatase activity throughout the whole culture phase.Cells of the transformed lines isolated by trypsin selection 2-6 months after infection displayed these properties when the cell density became high and cell growth was arrested.In the cells of the latter type of transformed lines, SV40 T-antigen was intensely demonstrated by immunofluorescence in the growing phase, but weakly or not at all in the stationary phase.It is suggested that the reversion to the phenotype of the progenitor (expression of macrophage specific functions ) depends on the physiological state of the culture; however, it is uncertain whether the development of the macrophage functions is directly related to the SV40 T-antigen.

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“…The anti-inflammatory effect of glucocorticoids is partially explained by their inhibitory effect on the migration of macrophages to the inflammation site (29). Macrophages accumulating at a local site will also increase by cell division (25). In our study, mouse macrophages obtained from a peritoneal inflammation site had an enhanced ability to multiply in response to a growth factor produced by mouse fibroblasts, compared with that of normal peritoneal macrophages (Fig.…”

Section: Discussionmentioning

confidence: 62%

Cell Growth and Antimicrobial Activity of Mouse Peritoneal Macrophages in Response to Glucocorticoids, Choleragen and Lipopolysaccharide

Nozawa

Yanaki

Yokota

1980

Microbiology and Immunology

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Normal, thioglycollate-stimulated and BCG-activated mouse peritoneal macrophages were cultivated in vitro with the conditioned medium of mouse L-929 cells. The thioglycollateand BCG-macrophages rapidly proliferated, whereas normal macrophages grew more slowly. A clear morphological difference between the three types of macrophages in the culture was observed.Glucocorticoids inhibited the growth of the macrophages at pharmacological concentrations. Other steroids, progesterone, diethylstilbesterol and testosterone in that order, had a far lower growth-inhibiting effect. Macrophages cultured with 10-6 M dexamethasone had a reduced antimicrobial effect on Candida parapsilosis compared with that of the untreated cells. Choleragen had the same effect on the macrophages as glucocorticoids. The toxin inhibited growth at a concentration as low as 10 pg/ml and cells treated with 1 ng of choleragen per ml had decreased antifungal activity. Similarly, Escherichia coli lipopolysaccharide at 10 ng/ml inhibited the growth of thioglycollate-macrophages.However, macrophages incubated with the lipopolysaccharide had enhanced anticandida activity. Thus, the immunosuppressors glucocorticoid and choleragen inhibited both the increase in the number of macrophages and the microbicidal activity of the phagocytes. Lipopolysaccharide, an immunostimulant, stimulated macrophage activity, but was toxic for cell growth.The mononuclear phagocytes in blood (monocytes) and tissues (macrophages) play a variety of important roles in host defense responses. One mechanism for controlling the responses due to mononuclear phagocytic (MP) cells is activation of MP cells in the host, for example, by infection with certain bacteria (13). Activated MP cells enhance a variety of cellular functions including killing of intracellular pathogens (12, 21) and cytotoxicity to tumor cells (3,9,20). Another mechanism may be the control of the absolute number of MP cells in vivo. The number of MP cells at a local inflammation site increases not only by the migration of blood monocytes (26, 27) but also by the proliferation of the migrated cells at the inflammation site, probably depending on a growth factor produced by lymphocytes or by fibroblasts, as evidenced in vitro (5,8,11,24).

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Proliferative capacity of mouse peritoneal macrophages in vitro.

Cited by 52 publications

References 25 publications

Macrophage-colony forming cells (M-CFC), with different sensitivities to colony stimulating factors, from peritoneal exudates and tissues of chronically inflamed mice

Macrophage-colony forming cells (M-CFC), with different sensitivities to colony stimulating factors, from peritoneal exudates and tissues of chronically inflamed mice

Transformation of Mouse Peritoneal Macrophages and Bone Marrow Cells by Simian Virus 40

Cell Growth and Antimicrobial Activity of Mouse Peritoneal Macrophages in Response to Glucocorticoids, Choleragen and Lipopolysaccharide

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