Properties of the Factor Increasing Monocytopoiesis (FIM) in Rabbit Peripheral Blood

Sluiter, Willem; Elzenga-Claasen, I; Hulsing-Hesselink, E.; Furth, R. van

doi:10.1007/978-1-4684-4394-3_17

Cited by 3 publications

(4 citation statements)

References 4 publications

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“…However, the intravenous injection of serum containing FIM into low responder CBA mice did not induce a response, whereas in high responder B10 mice, monocytosis was evoked. In neither of the strains did the course of granulocytes and lymphocytes change significantly after the injection of serum containing FIM, in accordance with the cell lineage-specific effect of FIM (3,5). Since a numerical increase of monocytes after the injection of serum containing FIM reflects increased monocyte production (3,5), we concluded that only high responder mice are able to respond to FIM by increased monocyte production.…”

Section: Discussionmentioning

confidence: 52%

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Differences in the response of inbred mouse strains to the factor increasing monocytopoiesis.

Sluiter¹,

Elzenga-Claasen²,

Andel³

et al. 1984

The Journal of Experimental Medicine

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Previous studies have shown that monocyte production during an inflammatory response is controlled by the factor increasing monocytopoiesis (FIM), secreted by macrophages at the site of inflammation. The inflammatory reaction to latex particles and a saline-soluble extract of Listeria monocytogenes (SEL), expressed as the number of monocytes in the circulation and of macrophages at the site of inflammation, was about twice as strong in C57BL/10 mice compared with CBA mice. This raised the question as to the mechanism underlying these differences. One possibility might be that these mouse strains differ with respect to the production of FIM, but this cannot be the case because the maximum levels of FIM activity in the serum of both C57BL/10 and CBA mice given latex or SEL intraperitoneally were almost the same; however, the courses of FIM activity in the two strains after intraperitoneal latex were not exactly synchronous. Another possibility is that the sensitivity of monocyte precursor cells for FIM differs. Evidence for the latter was provided by the finding that the intravenous injection of sera with FIM activity obtained from C57BL/10 and from CBA mice into the C57BL/10 mice evoked monocytosis, whereas CBA mice did not respond to these sera. Earlier studies showed that an increase of monocytes after the injection of serum containing FIM reflects increased monocyte production. Taken together, the results of the present study demonstrate that one of the mechanisms underlying the genetic control of the inflammatory response is, rather than enhanced FIM synthesis, the ability of monocyte precursors in the bone marrow to respond to FIM by increased monocyte production.

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Section: Discussionmentioning

confidence: 52%

“…mice were kept singly in cages and allowed to acclimate to the new environment (5). In each experiment, the animals were matched for age and handled in a random order.…”

mentioning

confidence: 99%

Differences in the response of inbred mouse strains to the factor increasing monocytopoiesis.

Sluiter¹,

Elzenga-Claasen²,

Andel³

et al. 1984

The Journal of Experimental Medicine

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“…Earlier investigations (3,5,8) had indicated that the factor increasing monocytopoiesis (FIM), present in the serum of mice and rabbits during the onset of an inflammatory response, is released by cells of the inflammatory exudate. The present study was performed to determine which cells produce and secrete this factor and to establish the kinetics of its production and secretion .…”

Section: Discussionmentioning

confidence: 99%

Macrophages as origin of factor increasing monocytopoiesis.

Sluiter

Hulsing-Hesselink

Elzenga-Claasen

et al. 1987

The Journal of Experimental Medicine

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Earlier investigations had indicated that the factor increasing monocytopoiesis (FIM), present in the serum of mice and rabbits during the onset of an inflammatory response, is released by cells of the inflammatory exudate. The present study was performed to determine which cells produce and secrete this factor and to establish the kinetics of its production and secretion. FIM was assayed in vivo by intravenous injection of samples into untreated mice and monitoring the course of the number of blood monocytes in the recipients. FIM was assayed in vitro by adding samples to cultures of the macrophage cell line PU5 and determining the rate of proliferation of the cells. The results show that only macrophages contain and synthesize FIM. This factor is secreted upon exposure to a phagocytic stimulus, and after the release of preformed FIM, macrophages secrete newly synthesized FIM. Granulocytes and lymphocytes neither contain nor secrete FIM. The characteristics of FIM derived from macrophages are in all aspects similar to those of FIM in serum. Macrophage-derived FIM is a protein with a molecular weight between 10 and 25 X 10(3), its activity is cell-lineage specific and dose dependent, and it stimulates monocyte production in the bone marrow. Macrophage-derived FIM is not identical to either CSF-1 or IL-1, and has no chemotactic activity. Taken together, the present results show that FIM occurring in serum during an inflammatory response originates from macrophages at the site of the inflammation. In this way the macrophages themselves regulate the supply of circulating blood monocytes that can migrate to the site of injury when needed.

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“…Recent investigations have shown that plasma and sera collected during the onset of an inflammatory reaction contain a factor that stimulates monocytopo iesis [12][13][14]. This factor, called factor-increasing monocytopoiesis (FIM), is synthesized and secreted by macrophages at the site of inflammation and then transported via the circulation to the bone marrow, where it exerts its stimulatory action (Fig.…”

Section: Origin and Kineticsmentioning

confidence: 99%