Organ-specific hematopoietic changes induced by a recombinant human interferon-? in mice

Rosenthal, Gary J.; Stranahan, Robert P.; Thompson, Miles D.; Blair, Patricia; Germolec, Dori R.; Comment, Christine E.; Schwab, Kellogg J.; Luster, Michael I.

doi:10.1016/0272-0590(90)90292-r

Cited by 14 publications

(7 citation statements)

References 18 publications

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“…IFNa rapidly reduced platelet and WBC counts and corrected erythrocytosis and splenomegaly according to disease severity. This is in agreement with previous studies in normal mice showing that IFNa impaired lymphopoiesis 45 as well as myelopoiesis, 46 inducing anemia, leukopenia, and thrombocytopenia.…”

Section: Discussionsupporting

confidence: 83%

JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFNα

Hasan

Lacout

Marty

et al. 2013

Blood

131

124

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Section: Discussionsupporting

confidence: 83%

JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFNα

Hasan

Lacout

Marty

et al. 2013

Blood

131

124

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“…In particular, HIV-infected macrophages and bone marrow microvascular endothelial cells, a key element of the stroma, could account for the regenerative failure and the reduced capacity to support on-demand myelopoiesis. This could result from the release of inappropriate growth factors or the upregulation of inhibitory cytokines such as tumor necrosis factor alpha and TGF-␤ (31,39).…”

Section: Discussionmentioning

confidence: 99%

Early and Persistent Bone Marrow Hematopoiesis Defect in Simian/Human Immunodeficiency Virus-Infected Macaques despite Efficient Reduction of Viremia by Highly Active Antiretroviral Therapy during Primary Infection

Thiébot

Louache

Vaslin

et al. 2001

J Virol

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The hematological abnormalities observed in human immunodeficiency virus (HIV)-infected patients appear to be mainly due to bone marrow dysfunction. A macaque models of AIDS could greatly facilitate an in vivo approach to the pathogenesis of such dysfunction. Here, we evaluated in this model the impact of infection with a pathogenic simian/human immunodeficiency virus (SHIV) on bone marrow hematopoiesis. Three groups of macaques were inoculated with 50 50% median infective doses of pathogenic SHIV 89.P, which expresses env of dual-tropic HIV type 1 (HIV-1) 89.6 primary isolate. During the primary phase of infection, animals were treated with either a placebo or highly active antiretroviral therapy (HAART) combining zidovudine, lamivudine, and indinavir, initiated 4 or 72 h postinfection (p.i.) and administered twice a day until day 28 p.i. In both placebo-treated and HAART-treated animals, bone marrow colony-forming cells (CFC) progressively decreased quite early, during the first month p.i. One year p.i., both placebo-and HAART-treated animals displayed decreases in CFC to about 56% of preinfection values. At the same time, a dramatic decrease (greater than 77%) of bone marrow CD34؉ long-term culture-initiating cells was noted in all animals were found. No statistically significant differences between placebo-and HAART-treated monkeys were found. These data argue for an early and profound alteration of myelopoiesis at the level of the most primitive CD34 ؉ progenitor cells during SHIV infection, independently of the level of viremia, circulating CD4 ؉ cell counts, or antiviral treatment.

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“…18.2 ± 0.9 (9) 19.9 ± 1.6 (9) (additive)0 16.9 ± 1.1 (10) 19 Table 1 '23) showed that the protective effect was synergistically enhanced in three of four experiments and in the summated data. Figure 1A presents the summated survival curves for mice treated with i.p.…”

mentioning

confidence: 94%

Orally Administered IFN-α Acts Alone and in Synergistic Combination with Intraperitoneally Administered IFN-γ to Exert an Antitumor Effect Against B16 Melanoma in Mice

Fleischmann

Masoor²,

Wu³

et al. 1998

Journal of Interferon & Cytokine Research

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Administration of interferons (IFN) via the intranasal route recently has been shown to exert an antitumor activity against a variety of tumors in mice, including B16 melanoma inoculated intravenously. This study confirms the antitumor activity of orally administered IFN-alpha against B16 melanoma challenge using another route of tumor inoculation, the intraperitoneal route. It further demonstrates that orally administered IFN-alpha can synergistically interact with intraperitoneally administered IFN-gamma but not with intraperitoneally administered IFN-alpha. The results support the interpretation that the oral route may provide an effective alternative or supplement to current methods of IFN administration for the control of malignancies.

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Organ-specific hematopoietic changes induced by a recombinant human interferon-? in mice

Cited by 14 publications

References 18 publications

JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFNα

JAK2V617F expression in mice amplifies early hematopoietic cells and gives them a competitive advantage that is hampered by IFNα

Early and Persistent Bone Marrow Hematopoiesis Defect in Simian/Human Immunodeficiency Virus-Infected Macaques despite Efficient Reduction of Viremia by Highly Active Antiretroviral Therapy during Primary Infection

Orally Administered IFN-α Acts Alone and in Synergistic Combination with Intraperitoneally Administered IFN-γ to Exert an Antitumor Effect Against B16 Melanoma in Mice

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