Erythropoietin enhances Kupffer cell number and activity in the challenged liver

Gilboa, Daniella; Haim-Ohana, Yasmin; Deshet-Unger, Naamit; Ben‐Califa, Nathalie; Hiram‐Bab, Sahar; Reuveni, Debby; Zigmond, Ehud; Gassmann, Max; Gabet, Yankel; Varol, Chen; Neumann, Drorit

doi:10.1038/s41598-017-11082-7

Cited by 40 publications

(32 citation statements)

References 80 publications

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“…However, contradictory phenomena were observed on resident macrophages. EPO can facilitate CCL2 production by Kupffer cells and promote the recruitment of monocytes to injured liver 29 . Similarly, increased levels of EPO can recruit more macrophages to laser-injured choroids 30 .…”

Section: Innate Immune System Macrophagementioning

confidence: 99%

Erythropoietin and its derivatives: from tissue protection to immune regulation

et al. 2020

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Erythropoietin (EPO) is an evolutionarily conserved hormone well documented for its erythropoietic role via binding the homodimeric EPO receptor (EPOR) 2. In past decades, evidence has proved that EPO acts far beyond erythropoiesis. By binding the tissue-protective receptor (TPR), EPO suppresses proinflammatory cytokines, protects cells from apoptosis and promotes wound healing. Very recently, new data revealed that TPR is widely expressed on a variety of immune cells, and EPO could directly modulate their activation, differentiation and function. Notably, nonerythropoietic EPO derivatives, which mimic the structure of helix B within EPO, specifically bind TPR and show great potency in tissue protection and immune regulation. These small peptides prevent the cardiovascular side effects of EPO and are promising as clinical drugs. This review briefly introduces the receptors and tissue-protective effects of EPO and its derivatives and highlights their immunomodulatory functions and application prospects.

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Section: Innate Immune System Macrophagementioning

confidence: 99%

Erythropoietin and its derivatives: from tissue protection to immune regulation

et al. 2020

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“…However, it cannot be excluded that hepatic EPO may be also involved in the stimulation of other processes in the liver, which are important to survive blood-stage malaria. For instance, EPO has been recently described to recruit Ly6C hi monocytes in response to liver injury [51] and to stimulate proliferation and phagocytotic activity of Kupffer cells-the liver-resident macrophages known for its capacity of erythrophagocytosing Plasmodiumparasitized red blood cells [11,12,[14][15][16]. Liver injury does also occur during blood-stage malaria in mice and even humans [11,52].…”

Section: Discussionmentioning

confidence: 99%

Vaccination accelerates hepatic erythroblastosis induced by blood-stage malaria

Delić

Wunderlich

Al‐Quraishy

et al. 2020

Malar J

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Background: Vaccination induces survival of otherwise lethal blood-stage infections of the experimental malaria Plasmodium chabaudi. Blood-stage malaria induces extramedullary erythropoiesis in the liver. This study investigates how vaccination affects the course of malaria-induced expression of erythrocytic genes in the liver. Methods: Female Balb/c mice were vaccinated at week 3 and week 1 before challenging with 10 6 P. chabaudi-parasitized erythrocytes. The non-infectious vaccine consisted of erythrocyte ghosts isolated from P. chabaudi-infected erythrocytes. Gene expression microarrays and quantitative real-time PCR were used to compare mRNA expression of different erythrocytic genes in the liver of vaccination-protected and non-protected mice during infections on days 0, 1, 4, 8, and 11 p.i. Results: Global transcriptomics analyses reveal vaccination-induced modifications of malaria-induced increases in hepatic gene expression on days 4 and 11 p.i. On these days, vaccination also alters hepatic expression of the erythropoiesis-involved genes Ermap,

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“…However, it cannot be excluded that hepatic EPO may be also involved in the stimulation of other processes in the liver, which are important to survive blood-stage malaria. For instance, EPO has been recently described to recruit Ly6C hi monocytes in response to liver injury [51] and to stimulate proliferation and phagocytotic activity of Kupffer cells -the liver-resident macrophages known for its capacity of erythrophagocytosing Plasmodium-parasitized red blood cells [11,12,[14][15][16]. Liver injury does also occur during blood-stage malaria in mice and even humans [11,52].…”

Section: Discussionmentioning

confidence: 99%

Vaccination accelerates hepatic erythroblastosis induced by blood-stage malaria

Delić

Wunderlich

Al‐Quraishy

et al. 2020

Preprint

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Background Vaccination induces survival of otherwise lethal blood-stage infections of the experimental malaria Plasmodium chabaudi . Blood-stage malaria induces extramedullary erythropoiesis in the liver. This study investigates how vaccination affects the course of malaria-induced expression of erythrocytic genes in the liver. Methods Female Balb/c mice were vaccinated at week 3 and week 1 before challenging with 10 6 P. chabaudi- parasitized erythrocytes. The non-infectious vaccine consisted of erythrocyte ghosts isolated from P. chabaudi -infected erythrocytes. Gene expression microarrays and quantitative real-time PCR were used to compare mRNA expression of different erythrocytic genes in the liver of vaccination-protected and non-protected mice during infections on days 0, 1, 4, 8, and 11 p.i. . Results Global transcriptomics analyses reveal vaccination-induced modifications of malaria-induced increases in hepatic gene expression on days 4 and 11 p.i.. On these days, vaccination also alters hepatic expression of the erythropoiesis-involved genes Ermap, Kel, Rhd , Rhag , Slc4a1, Gypa, Add2, Ank1, Epb4.1, Epb4.2, Epb4.9, Spta1, Sptb, Tmod1 , Ahsp, Acyp1 , Gata1, Gfi1b, Tal1, Klf1, Epor , and Cldn13 . In vaccination-protected mice, expression of these genes, except Epb4.1 , is significantly higher on day 4 p.i. than in un-protected non-vaccinated mice, reaches maximal expression at peak parasitaemia on day 8 p.i., and is slowed down or even decreased towards the end of crisis phase on day 11 p.i.. After day 1 p.i., Epor expression takes about the same course as that of the other erythroid genes. Hepatic expression of Epo, however, is delayed in both vaccinated and non-vaccinated mice for the first 4 days p.i. and is maximal at significantly higher levels in vaccinated mice on day 8 p.i. , before declining towards the end of crisis phase on day 11 p.i. . Conclusion The present data indicate that vaccination accelerates malaria-induced erythroblastosis in the liver for 1-2 days. This may contribute to earlier replenishment of peripheral red blood cells by liver-derived reticulocytes, which may favour final survival of otherwise lethal blood-stage malaria, since reticulocytes are not preferred as host cells by P. chabaudi .

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Erythropoietin enhances Kupffer cell number and activity in the challenged liver

Cited by 40 publications

References 80 publications

Erythropoietin and its derivatives: from tissue protection to immune regulation

Erythropoietin and its derivatives: from tissue protection to immune regulation

Vaccination accelerates hepatic erythroblastosis induced by blood-stage malaria

Vaccination accelerates hepatic erythroblastosis induced by blood-stage malaria

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