Role of mast cells in reactions of the blood system during inflammation

Klimenko, N. A.; Дыгай, А. М.; Abramova, Elena; Симанина, Е. В.; Gumilevskii, B. Yu.; Boldyshev, D. A.; Gol'dberg, E. D.

doi:10.1007/bf00840620

Cited by 3 publications

(7 citation statements)

References 8 publications

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“…However, despite the more strained functioning of local regulatory mechanisms of erythropoiesis, hyperplasia characteristic of natural inflammation did not develop. This is consistent with the absence of marked hyperplasia of the granulomonocytic series in the bone marrow in inflammation induced in the absence of mast ceils, despite a more pronounced early activation of HIM and stimulation of granulomonocytopoiesis [4,5].…”

Section: Resultssupporting

confidence: 70%

“…It fias been previously found that inflammation in the absence of mast cells is characterized by a delayed rise of colony-stimulating activity in the blood [5]. Since EPA and colony-stimulating activity in inflammation are also provided by activated monocytederived macrophages [8], the delayed rise of EPA and colony-stimulating activity in the blood can be attributed to inhibited migration and reduced functional activity of monocytes in the inflammation focus and in the blood [4,6].…”

Section: Resultsmentioning

confidence: 94%

“…Experiments were carried out on 204 male CBA mice weighing 18-20 g. The model of inflammation was infectious peritonitis caused by Escherichia coli strain ATCC 25922 inoculated intraperitoneally in 0.3 ml isotonic NaC1 solution in a dose of 0.5 LDs0 [4]. The mice were decapitated at various times of the inInstitute of Pharmacology, Tomsk Research Center, Russian Academy of Medical Sciences; *State Medical University, Kharkov flammatory process, and the total number of myelokaryocytes per femur and myelogram were counted.…”

Section: Methodsmentioning

confidence: 99%

“…Our previous studies show that must cells modulate the intensity of granulomonocytopoiesis during inflammation [4]. It was also shown that inflammation characterized by marked stimulation of erythropoiesis and on days 6-9 of inflammation by hyperplasia of erythron in_ the bone marrow due to activation of proliferation and differentiation of committed erythropoiesis precursors, hemopoiesis-inducing microenvironment (HIM) of the bone marrow, and the erythropoietin system [2].…”

Section: Abstract: Inflammation; Erythropoiesis; Mast Cellsmentioning

confidence: 97%

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Role of mast cells in regulation of erythropoiesis during inflammation

et al. 1997

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Using the mouse model of acute infectious peritonitis caused by Escherichia coli, we have shown that preliminary osmotic elimination of peritoneal mast cells markedly affects the erythron reaction and its mechanisms during inflammation. Activation of local regulatory mechanisms of erythropoiesis (hemopoiesis-inducing microenvironment) and less pronounced hyperplasia of the erythron in the bone marrow were noted. Key Words: inflammation; erythropoiesis; mast cellsOur previous studies show that must cells modulate the intensity of granulomonocytopoiesis during inflammation [4]. It was also shown that inflammation characterized by marked stimulation of erythropoiesis and on days 6-9 of inflammation by hyperplasia of erythron in_ the bone marrow due to activation of proliferation and differentiation of committed erythropoiesis precursors, hemopoiesis-inducing microenvironment (HIM) of the bone marrow, and the erythropoietin system [2].The aim of the present study was to evaluate the role of mast ceils in the regulation of erythropoiesis in inflammation. MATERIALS AND METHODSExperiments were carried out on 204 male CBA mice weighing 18-20 g. The model of inflammation was infectious peritonitis caused by Escherichia coli strain ATCC 25922 inoculated intraperitoneally in 0.3 ml isotonic NaC1 solution in a dose of 0.5 LDs0 [4]. The mice were decapitated at various times of the inInstitute of Pharmacology, Tomsk Research Center, Russian Academy of Medical Sciences; *State Medical University, Kharkov flammatory process, and the total number of myelokaryocytes per femur and myelogram were counted. In the bone marrow, committed erythropoietic precursors, erythroid colony-forming units (CFU-E) [10], and hemopoietic islets [1,9] were counted, and erythropoietic activity of blood serum and conditioned media of adherent and nonadherent bone marrow cells was determined [12]. Conditioned media were obtained by culturing adherent or nonadherent myelokaryocytes (2 x 106 cells/ml) in complete RPMI-1640 medium supplemented with 10% fetal bovine serum for 24 h in the presence of 10 gg/ml lipopolysaccharide from E. coli serotype 01 l l:B4 (Sigma) or 5 gg/ml concanavalin A (ConA, Sigma). Mast cells were eliminated by intraperitoneal injection of 1.8-2 ml distilled water 10 days before peritonitis [7,11]. RESULTSNatural inflammation was characterized by a shortterm rise of erythroid elements in the bone marrow by hour 12 and hyperplasia of the erythron on days 6-9. In the absence of mast cells, the number of erythrokaryocytes rose considerably on day 1 (Fig. 1, a), i.e., erythron hyperplasia practically did not develop.

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Section: Resultssupporting

confidence: 70%

Section: Resultsmentioning

confidence: 94%

Section: Methodsmentioning

confidence: 99%

Section: Abstract: Inflammation; Erythropoiesis; Mast Cellsmentioning

confidence: 97%

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Role of mast cells in regulation of erythropoiesis during inflammation

et al. 1997

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“…The experiment was carried out on 102 male CBA mice weighing 18-20 g. The model of inflammation was infectious peritonitis caused by Escherichia coli strain ATCC 25922 inoculated intraperitoneaUy in Institute of Pharmacology, Tomsk Research Center, Russian Academy of Medical Sciences; Medical Institute, Kharkov 0.3 ml isotonic NaC1 solution in a dose equal to one-half of the LDs0 [4,7]. Mice were killed by decapitation at various times of the inflammatory process, and the total number of myelokaryocytes was counted in the femur and a myelogram prepared.…”

Section: Methodsmentioning

confidence: 99%

On the erythron response to inflammation and its mechanisms

et al. 1995

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Using the mouse model of acute infectious peritonitis caused by Escherichia coli, it isshown that the development of inflammation is accompanied by increases in the number of erythrokaryocytes, erythroid colony-forming units, and erythroid hematopoietic islets in the bone marrow and by rises in the activities of supernatants of cultured stimulated adherent and nonadherent myelokaryocytes and of peripheral blood. The results of this study indicate that a characteristic feature of acute inflammation is strong activation of erythropoiesis with the development of hyperplasia of the erythroid marrow. Key Words: inflammation; erythropoiesisThe mechanisms underlying the regulation of erythropoiesis in inflammation have been studied inadequately, and the available information about quantitative changes in the erythron during inflammatory processes is scanty and contradictory. There are reports of anemia with a fall in the number of erythroid cells in the bone marrow occurring as early as 24 h after the experimental induction of acute inflammation and peaking on days 6-9 [1,2,8], and erythrocytosis has been found to develop at the same times [6].The present experiment was undertaken to investigate the response of the erythron to acute inflammation and the mechanisms of this response. MATERIALS AND METHODSThe experiment was carried out on 102 male CBA mice weighing 18-20 g. The model of inflammation was infectious peritonitis caused by Escherichia coli strain ATCC 25922 inoculated intraperitoneaUy in

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Role of mast cells in reparative processes in inflammation

Klimenko¹,

Татарко²

1995

Bull Exp Biol Med

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Using the model of acute infectious peritonitis in rats, it is shown that inflammation induced in the absence of mast cells is characterized by marked inhibition of reparative processes. The most significant accumulation of functionally active fibroblasts and the development of granulations and young connective tissue in the mesentery occur 5-10 days after flogogen injection in the natural development of inflammation and after 10-20 days in the absence of mast cells. The data suggest that under natural conditions mast cells directly or indirectly stimulate reparative processes. Key Words: inflammation; mast cells; repairAt present, mast ceils (MC) are considered to be the source of the main transmitters of initial vascular and exudative processes, in particular the immediate phase of the increase of vascular permeability [8,9] underlying exudation. Recently, a modulatory effect of MC on infdtration processes during inflammation has been shown and mechanisms of this effect dependent on the main products of MC, histamine, serotonin, and heparin, have been studied [6,7].The aim of the present study was to investigate the role of MC in reparative processes during inflammation. MATERIALS AND METHODSThe experiments were performed on 396 male Wistar rats weighing 180-200 g. Acute infectious peritonitis was induced by intraperitoneal injection of 2x109 cells (0.5 LDs0 ) of a one-day-old E. coli culture, isolated from a patient with peritonitis, in 1 ml isotonic NaC1 [5,7,8]

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Role of mast cells in reactions of the blood system during inflammation

Cited by 3 publications

References 8 publications

Role of mast cells in regulation of erythropoiesis during inflammation

Role of mast cells in regulation of erythropoiesis during inflammation

On the erythron response to inflammation and its mechanisms

Role of mast cells in reparative processes in inflammation

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