FURTHER STUDIES ON MOBILIZATION OF CFUs

Vos, O.; Wilschut, Ina J. C.

doi:10.1111/j.1365-2184.1979.tb00148.x

Cited by 14 publications

(13 citation statements)

References 16 publications

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“…[32][33][34] We therefore hypothesized that low levels of endotoxins passing through the intestinal mucosa into the blood may contribute to the levels of circulating HPCs. Here, we used a mouse model to study the effects of selective antibiotic decontamination on cytokine-induced stem cell mobilization.…”

Section: Introductionmentioning

confidence: 99%

“…Endotoxins are also known as potent inducers of mobilization following systemic administration. 32,33 Under clinical and experimental conditions the lipopolysaccharide component of the aerobic Gram-negative bacteria wall damages the endothelial cell 48 finally leading to the synthesis and the release of proinflammatory mediators (TNF, IL-1, IL-6, and IL-8) from macrophages. 49 The endotoxin concentration in the gut is very likely to be decreased by the treatment with polymyxin B or metronidazol, resulting in a diminished production of cytokines by macrophages.…”

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confidence: 99%

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Reduced stem cell mobilization in mice receiving antibiotic modulation of the intestinal flora: involvement of endotoxins as cofactors in mobilization

Velders

Hagoort

et al. 2004

Blood

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IntroductionTo reduce the risk of infections in neutropenic patients a combination of protective isolation and gut decontamination by oral administration of antibiotics is often used. [1][2][3][4] Since it has been shown that selective elimination of the major potentially pathogenic microorganisms from the digestive tract is as effective or even superior to total decontamination in preventing infections in neutropenic patients, 5-8 selective gut decontamination 9 or partial antibiotic decontamination 10 mainly directed against aerobic Gram-negative rods and fungi is usually applied. The various antibiotics used for selective decontamination can be divided into 2 main groups, those that are absorbed 11-13 after oral administration (eg, cotrimoxazole, quinolones) and those that are not absorbed 2-4 after oral administration (eg, polymyxin, colistin, aminoglycosides).Mobilized hematopoietic progenitor cells (HPCs) are increasingly used for hematopoietic recovery instead of bone marrow to allow rapid hematopoietic recovery after autologous and allogeneic transplantation. [14][15][16][17][18] An increasing number of different growth factors and chemokines such as granulocyte colony-stimulating factor (G-CSF), 19,20 granulocyte-macrophage colony-stimulating factor (GM-CSF), 19,21 stem cell factor (SCF), 22 flt3 ligand (FL), 23 interleukin-1 (IL-1), 24 26 and thrombopoietin 27 when either administered alone or in combination 28 are capable of mobilizing peripheral blood progenitor cells. In the clinical setting, the growth factor G-CSF has become the standard for autologous as well as allogeneic peripheral blood stem cell transplantation. [29][30][31] Although patients receiving selective gut decontamination or systemic antibiotic treatment while concurrently being treated with G-CSF are able to mobilize peripheral blood progenitor cells, little is known of the effect of antibiotics on the efficacy of mobilization.Endotoxins are ubiquitously present and constitute an important component of the normal intestinal flora and are known to induce HPC mobilization. [32][33][34] We therefore hypothesized that low levels of endotoxins passing through the intestinal mucosa into the blood may contribute to the levels of circulating HPCs. Here, we used a mouse model to study the effects of selective antibiotic decontamination on cytokine-induced stem cell mobilization. We found that the ability to mobilize in response to IL-8, G-CSF, or FL was significantly reduced in animals receiving endotoxin binding antibiotics or antibiotics that modulate the anaerobic flora. The mobilizing capacity was partially restored after adding endotoxins to the drinking water of decontaminated mice. These observations indicate that endotoxins are involved as cofactors in cytokineinduced hematopoietic stem cell mobilization. Supported by a grant from the Fund for Scientific Research FWO-Vlaanderen, the "Geconcerteerde Onderzoeks Acties" (GAO), and by the Dutch Cancer Society (NKB-RUL 99-2029).Reprints: Willem E. Fibbe, Department of Hematology, Lei...

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Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

Reduced stem cell mobilization in mice receiving antibiotic modulation of the intestinal flora: involvement of endotoxins as cofactors in mobilization

Velders

Hagoort

et al. 2004

Blood

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“…This hypothesis is unlikely in view of the marked and selective enhancement of BFU-E proliferation and the dramatic increase of their pools in blood and spleen. It must be pointed out, however, that migration of both early hemopoietic precursors and stem cells is not restricted to leukemic diseases but has also been reported in stress erythropoiesis (11) and after injection of zymosan (17). On the other hand, in view of the fact that the BFU-E is closely related to the CFU-S (18), the possibility should be considered in future studies that the latter also represents a target cell for FLV.…”

Section: Discussionmentioning

confidence: 99%

“…1 and 3B). On the other hand, in FLV-A-infected mice, the plateau phase of BFU-E in the blood on days [10][11][12][13][14][15][16][17][18][19][20] was associated with a decrease in the number of BFU-E in the spleen, apparently due to differentiation of BFU-E to CFU-E (Figs. 1 and 2B).…”

Section: Clonal Analysis Of Erythroid Precursors In Marrowmentioning

confidence: 99%

Kinetics of erythroid precursors in mice infected with the anemic or the polycythemic strain of Friend leukemia virus

Peschle

Migliaccio

Lettieri

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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The kinetics of both erythroid burst-forming and colony-forming units (BFU-E, CFU-E) and myelomonocytic precursors [myelomacrophage colony-forming unit (CFU-C)J have been evaluated in tibial marrow, peripheral blood, and spleen of DBA/2 mice at time intervals after inoculation of either the anemic (FLy-A) or the polycythemic (FLV-P) strain of Friend leukemia virus. Either one of the viruses induced, at 7-10 days after infection, a massive increase in the number of BFU-Es in peripheral blood, in parallel with their depletion in tibial marrow and increase in spleen. A comparable increase in the blood BFU-E number was observed in splenectomized FLV-infected mice. These results indicate a marrow-spleen migration of BFU-Es. In spleen, the increase of the BFU-E number was associated with an increase in the CFU-E pool. In tibial marrow, a sequence of expansion/depletion waves occurred reciprocally at the level of BFU-E and CFU-E. The cycling of BFLT-E ([3Hthymidine in vitro suicide index) in marrow, blood, and spleen was enhanced, whereas that of CFU-E and CFU-C showed little or no modification. These kinetic data suggest that the main target cell of FLV may be the BFU-E or a closely related element. In plates without added erythropoietin (but containing it in fetal calf serum), expression of CFU-E from FLV-P-treated animals was maximal; that of CFU-E from FLV-A-injected mice was either virtually absent or only slight in marrow or spleen, respectively. BFU-E growth always was fully dependent upon erythropoietin addition. Control studies in FLV-infected resistant mice and in susceptible mice given diluted or heat-inactivated virus provide convincing evidence that the phenomena described are induced by FLV.

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“…At lower doses it induces a biphasic mobilization of haemopoietic progenitor cells and the production of auto-antibodies and circulating immune complexes (CICs) [Vos et al, 1972;Vos and Wilschut, 1979;Cun ningham, 1974;Fournié et al, 1974;Izui et al, 1977a;Rose et al, 1982;Bloembergen et al, 1987].…”

Section: Introductionmentioning

confidence: 99%

Endotoxin-Induced Auto-Immunity in Mice

Bloembergen¹,

Dijk²,

Hofhuis³

et al. 1988

Int Arch Allergy Immunol

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Auto-antibody responses and circulating immune complex levels of mice with abnormal reactions to endotoxin were investigated after injection with the bacterial product. It was observed that C3H/HeJ mice displayed very high background plaque-forming cell responses towards bromelain-treated isologous erythrocytes which were slightly enhanced by endotoxin treatment. The same animals, however, did not bear auto-haemolysins in their serum, but became so upon endotoxin injection. A possible relationship between the high background reactivity of C3H/HeJ mice and the low toxicity of endotoxin in these animals is discussed. Neither untreated nor lipopolysaccharide-injected C3H/HeJ mice showed significant immune complex levels in their sera. This may be explained by their hyporesponsiveness, but by a low sensitivity to the toxic effects of endotoxin as well. C5-deficient and C5-sufficient mice showed similar auto-immune reactions, indicating that C5a, which is responsible for other effects of endotoxin, is not involved in endotoxin-induced auto-immunity.

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FURTHER STUDIES ON MOBILIZATION OF CFUs

Cited by 14 publications

References 16 publications

Reduced stem cell mobilization in mice receiving antibiotic modulation of the intestinal flora: involvement of endotoxins as cofactors in mobilization

Reduced stem cell mobilization in mice receiving antibiotic modulation of the intestinal flora: involvement of endotoxins as cofactors in mobilization

Kinetics of erythroid precursors in mice infected with the anemic or the polycythemic strain of Friend leukemia virus

Endotoxin-Induced Auto-Immunity in Mice

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