Effect of Endotoxin on Serum Granulocyte and Granulocyte-Macrophage Colony-Stimulating Factor Levels in Dogs

Dale, David C.; Lau, Stella; Nash, Richard A.; Boone, T.; Osborne, William

doi:10.1093/infdis/165.4.689

Cited by 31 publications

(15 citation statements)

References 15 publications

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“…Bioactivity of virally expressed canine G-CSF was monitored using a murine cell line, NFS-60, that proliferates in response to G-CSF. 43 Recombinant canine G-CSF (Amgen, Thousand Oaks, CA) was used to construct a proliferation-response curve with murine NFS-60 cells. 43,44 Proliferation was assayed by a commercial dye production assay (Cell Titer 96; Promega, Madison, WI).…”

Section: G-csf Production In Vitromentioning

confidence: 99%

“…43 Recombinant canine G-CSF (Amgen, Thousand Oaks, CA) was used to construct a proliferation-response curve with murine NFS-60 cells. 43,44 Proliferation was assayed by a commercial dye production assay (Cell Titer 96; Promega, Madison, WI). In brief, NFS-60 cells seeded at a concentration of 10 5 cells/well in 96-well microtiter plates were cultured for 24 hours at 37°C, 5% CO 2 .…”

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confidence: 99%

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Treatment of canine cyclic neutropenia by lentivirus-mediated G-CSF delivery

Yanay

Barry

Katen

et al. 2003

Blood

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Cyclic neutropenia is a rare disease that occurs both in humans and gray collie dogs and is characterized by recurrent severe neutropenia leading to bacterial infections and shortened life expectancy. Daily injections of recombinant granulocyte colony-stimulating factor (rG-CSF) are effective in shortening the period of severe neutropenia and reducing infections. After demonstrating that rG-CSF induced elevated neutrophil production in an affected dog, cytokine administration was stopped and 10 9 infectious units (IUs) of a lentivirus pseudotyped with vesicular stomatitis virus G protein (VSV-G) encoding canine G-CSF cDNA was administered intramuscularly. Serial blood cell counts showed elevated neutrophil production for longer than 17 months. Although neutrophil counts continued to cycle, the range at nadirs was from 3710 to 5300 cells/L, well above the nadirs before lentivirus administration. After the injection of lentivirus, mean neutrophil counts ؎ SD were 12 460 ؎ 4240 cells/ L, significantly increased over both pretreatment values of 3040 ؎ 2540 cells/L (P < .0001) and neutrophil counts during G-CSF administration of 10 290 ؎ 4860 cells/L (P < .007). The changes in blood counts from lentivirus injection were associated with absence of clinical signs of infection and fever. The gray collie continued to gain weight and was no longer housed in a pathogen-free environment. Genomic DNA from muscle at injection sites was positive for provirus, whereas gonad, lung, spleen, heart, liver, kidney, leukocytes, and noninjected muscle samples were all negative for provirus. Thus, intramuscular administration of lentivirus encoding G-CSF provided sustained therapeutic levels of neutrophils, suggesting this approach may be applied for long-term treatment of patients with cyclic and other neutropenias. IntroductionCyclic neutropenia is a rare disease that occurs both in man and gray collie dogs. In collie dogs, cyclic hematopoiesis is inherited as an autosomal recessive disease. 1,2 The dogs have 12-to 14-day cyclic variations in blood neutrophils, monocytes, lymphocytes, eosinophils, reticulocytes, and platelets due to periodic fluctuations in blood cell production by the bone marrow. 1,2 The recurrent severe neutropenia leads to bacterial infections and shortened life expectancy. The disorder can be cured by bone marrow transplantation from a normal dog to a gray collie as well as transferred from a gray collie to a normal littermate. 3,4 This transplantability strongly supports the concept that this is a disease of defective regulation of hematopoietic stem cells.Gray collie dogs with cyclic hematopoiesis have been successfully treated with granulocyte colony-stimulating factor (G-CSF). 5,6 The severe recurrent neutropenia in gray collie dogs was not abrogated by in vivo interleukin 3 (IL-3) or granulocytemacrophage colony-stimulating factor (GM-CSF) treatment. 5 In contrast, G-CSF prevented the recurrent neutropenia and obliterated periodic fluctuation of monocyte, eosinophil, reticulocyte, and platelet counts. 5,6 ...

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Section: G-csf Production In Vitromentioning

confidence: 99%

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confidence: 99%

Treatment of canine cyclic neutropenia by lentivirus-mediated G-CSF delivery

Yanay

Barry

Katen

et al. 2003

Blood

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“…One possibility might be stimulation from chronic endotoxin exposure as a consequence of the antimicrobial defect of the neutrophils. 14,15 We studied the possibility that bacterial infections (LPS) may trigger TNF␣ secretion in C/EBP⑀ −/− monocytes which could lead to increased serum G-CSF and/or GM-CSF levels. 16,17 Only one (4. month old) out of 10 mice had increased TNF␣ serum levels.…”

Section: Figurementioning

confidence: 99%

C/EBPε −/− mice: increased rate of myeloid proliferation and apoptosis

et al. 2001

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CCAAT/enhancer binding protein epsilon (C/EBP⑀) is essential for terminal granulocytic differentiation. Its expression begins at the transition between the proliferative and non-proliferative compartments of myelopoiesis. We studied the effect of targeted disruption of the C/EBP⑀ gene on murine myeloid proliferation and apoptosis. Bone marrow cellularity of C/EBP⑀ −/− and wild-type mice was 95% and 65%, respectively. The C/EBP⑀ −/− mice had an expansion in the number of their CFU-GM/femur. The number of myeloid committed progenitor cells in the peripheral blood and the spleen of these mice was also increased. Bromodeoxyuridine (BrDU) pulse labeling studies demonstrated that the fraction of actively proliferating cells was two-fold higher in the bone marrow of C/EBP⑀ −/− mice. However, the number of myeloid colonies arising from purified Sca-1+/lin− early hematopoietic progenitor cells and from bone marrow mononuclear cells grown in different cytokine combinations was not significantly different between wild-type and knock-out mice. Also, long-term marrow growth, and CFU were not different between the wild-type and C/EBP⑀ −/− mice. The sensitivity to induction of apoptosis in the committed progenitor cell compartment after either withdrawal of growth factor or brief exposure to etoposide was normal. However, Gr-1 antigen-positive C/EBP⑀ −/− granulocytic cells showed an increased rate of apoptosis in comparison to their wild-type counterparts. In summary, the myeloid compartment appears to be expanded in mice lacking C/EBP⑀. However, this is not the consequence of an intrinsic myeloproliferation but due to an indirect, possibly cytokine-mediated stimulation of myelopoiesis in vivo. C/EBP⑀ may have a role in the inhibition of apoptosis in maturing granulocytic cells. Leukemia (2001) 15, 103-111.

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“…Cytokine secretion ffom LrGSN-transduced cells was monitored using a murine cell line, NFS-60, that proliferates in response to G-CSF (Dale et al, 1992). Recombinant canine G-CSF (kindly supplied by Amgen, Thousand Oaks, CA) was used to constract a proliferation-response curve with murine NFS-60 cells (Dale et al, 1992).…”

Section: G-csf Bioassaymentioning

confidence: 99%

“…Recombinant canine G-CSF (kindly supplied by Amgen, Thousand Oaks, CA) was used to constract a proliferation-response curve with murine NFS-60 cells (Dale et al, 1992). In brief, short-tenn proliferation was determined by measuring tritiated thymidine incorporation by cells seeded at a concentration of 10' cells/well in 96-well microtiter plates.…”

Section: G-csf Bioassaymentioning

confidence: 99%