IL-6-induced anaemia in rats: possible pathogenetic implications for anaemia observed in chronic inflammations

Jongen‐Lavrencic, Mojca; Peeters, Harald; Rozemuller, Henk; Rombouts, W. J. C.; Martens, Anton C.; Vreugdenhil, Gerard; Pillay, Manormoney; Cox, Patricia; Bijser, M.; Brutel, G.; Breedveld, Ferdinand C.; Swaak, A. J. G.

doi:10.1046/j.1365-2249.1996.d01-622.x

Cited by 60 publications

(28 citation statements)

References 33 publications

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“…The infused dose provided 13 g of rhIL-6 per rat per day, and the total amount was calculated to last for 7 days. This daily dose was equivalent to that used in previous studies to induce hypoferremia without deleterious effects to experimental animals (30). Even larger doses would not have led to pathological changes in the liver or kidney (31).…”

Section: Discussionmentioning

confidence: 98%

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Gieng

Raila

Rosales

2005

Journal of Lipid Research

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We assessed the effects of prolonged reduction of plasma retinol concentrations (hyporetinolemia) on the distribution of tissue vitamin A (VA) and of its active compounds using a model of continuous recombinant human interleukin-6 (rhIL-6) infusion via osmotic minipumps in VAsufficient male rats. Plasma retinol and retinol-binding protein (RBP) concentrations remained decreased and lower in rhIL-6-treated rats compared with controls from 7.5 h throughout 7 days of infusion ( P Ͻ 0.001). This reduction was accompanied by a 68% increase in hepatic retinol concentration by 7 days ( P Ͻ 0.05). Hepatic and renal retinyl palmitate and retinoic acid concentrations did not change, and renal megalin content remained unchanged; hepatic RBP concentrations were 41% lower in rhIL-6-treated rats compared with controls ( P Ͻ 0.05). These results indicate that instead of being lost, retinol accumulated in the liver during inflammation and that hyporetinolemia was attributable to a decrease in the availability of hepatic RBP. A plausible consequence of the effect of rhIL-6-induced hyporetinolemia is that by 7 days tissues that are dependent on plasma retinol may become deprived of VA. These results have important implications in understanding the mechanism by which measles infection induces hyporetinolemia and VA deficiency of extrahepatic tissues. -Gieng, S. H., J. Raila, and F. J. Rosales. Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat. J. Lipid Res. 2005. 46: 641-649.

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Section: Discussionmentioning

confidence: 98%

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Gieng

Raila

Rosales

2005

Journal of Lipid Research

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“…Inflammation, infection, and injury also profoundly alter erythropoiesis and generally result in anemia. The pathogenesis behind alterations in erythropoiesis involves multiple factors, including cytokine-mediated erythroid apoptosis, a blunted BM response to erythropoietin, reduced iron availability, suppression of erythroid progenitor cell proliferation, and BM egress of erythroid progenitor cells (34,40,50,51). Infection and inflammation also modulate the numbers of platelets.…”

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confidence: 99%

Infection withAnaplasma phagocytophilumInduces Multilineage Alterations in Hematopoietic Progenitor Cells and Peripheral Blood Cells

et al. 2009

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Infection withHematopoietic lineage assessment demonstrated that there was loss of erythrocytes and B lymphocytes from the BM along with increased granulopoiesis. These changes were accompanied by splenomegaly due to lymphoid hyperplasia and increased hematopoiesis, most notably erythropoiesis. These changes largely mimic well-described inflammation and endotoxin-mediated effects on the BM and spleen; however, the numbers of peripheral blood neutrophils appear to be independently modulated as granulocytic hyperplasia does not result in neutrophilia. Our findings highlight a well-conserved series of events that we demonstrate can be instigated by an LPS-negative pathogen in the absence of an endotoxin-mediated acute proinflammatory response.

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“…Dysregulated activation of pro-inflammatory cytokines can lead to various inflammatory disorders [5]. In addition, experimental administration of both IL-6 and TNF-α to cattle induced the systemic inflammation, which is similar clinical sign to ECF [3,13]. This raises the possibility that the pro-inflammatory cytokines could be involved in the severity of the disease in T. parva-infected animals.…”

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confidence: 99%

Quantitative Analysis of Cytokine mRNA Expression and Protozoan DNA Load in Theileria parva-Infected Cattle

Yamada

Konnai

Imamura

et al. 2009

The Journal of Veterinary Medical Science

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ABSTRACT. Theileria parva (T. parva) causes a highly serious bovine disease called East Coast fever (ECF), which is characterized by pyrexia, dyspnea and cachexia and is of great economic importance in African countries. We hypothesize that the clinical symptoms of ECF could be explained by a cytokine dysregulation. In this study, we investigated the relationship between T. parva DNA load and expression levels of cytokine mRNAs in leukocytes from experimentally infected calves by quantitative PCR. The p104 gene, which encodes the T. parva 104 kDa microneme-rhoptry protein, was detected in cattle blood from day 10 after T. parva-infected tick infestation, and the protozoan DNA load was increased together with severity of disease. The mRNA expressions of pro-inflammatory cytokines, such as interleukin (IL)-1β and IL-6, were up-regulated with protozoan DNA load increasing. In addition, the level of a type-2 cytokine (IL-10) transcript was also increased during the acute phase. In contrast, the down-regulation or no detectable levels of the expression of type-1 cytokines, such as IL-2 and interferon (IFN)-γ were observed in T. parva-infected animals. Thus, our observations indicated that high protozoan load and resulting intense inflammatory responses might be involved in the severity of clinical signs observed in T. parva-infection.

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IL-6-induced anaemia in rats: possible pathogenetic implications for anaemia observed in chronic inflammations

Cited by 60 publications

References 33 publications

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Accumulation of retinol in the liver after prolonged hyporetinolemia in the vitamin A-sufficient rat

Infection withAnaplasma phagocytophilumInduces Multilineage Alterations in Hematopoietic Progenitor Cells and Peripheral Blood Cells

Quantitative Analysis of Cytokine mRNA Expression and Protozoan DNA Load in Theileria parva-Infected Cattle

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