scholarly journals G-CSF: A Vehicle for Communication Between Trophoblasts and Macrophages, Which May Cause Problems in Recurrent Spontaneous Abortion

2021 ◽  
Author(s):  
Peng Gao ◽  
Haiyi Liu ◽  
Ying Zha ◽  
Lijie Wei ◽  
Xuan Zhou ◽  
...  
Keyword(s):  
Spontaneous Abortion ◽  
Macrophage Activation ◽  
Cell Activity ◽  
Cell Communication ◽  
Recurrent Spontaneous Abortion ◽  
Granulocyte Colony Stimulating Factor ◽  
Pregnancy Failure ◽  
Normal Tissues ◽  
Key Factor ◽  
Stimulating Factor

Abstract Background: The etiology of about half of patients with recurrent spontaneous abortion (RSA) remains unclear. Imbalance of the immune inflammatory response at the mother-foetal interface may be one of the keys to the onset of RSA. Granulocyte-colony stimulating factor (G-CSF) is thought to have a protective effect on pregnancy and its absence may lead to pregnancy failure. However, the evidence of the described effects of G-CSF is scant. This study aimed at investigating whether the loss of G-CSF induced RSA by affecting cell communication at the maternal-foetal interface.Results: It was found that G-CSF was mainly expressed in villus rather than decidua and expression in RSA tissues was lower than that in normal tissues. Further, the down-regulation of G-CSF in trophoblasts resulted to a decrease in cell activity. Trophoblast-derived exosomes inhibited macrophage activation, while G-CSF free exosomes did not. Intraperitoneal injection of G-CSF improved the pregnancy outcome in RSA mice and the expression of G-CSF as well as its receptor at the mother-foetal interface were also changed.Conclusion: The expression of G-CSF was found to be decreased in villi of patients with RSA. It was evident that the absence of G-CSF weakens the immune suppression of trophoblasts against macrophages and the function of trophoblasts is also impaired. Therefore, this may be a key factor in the occurrence of RSA. Further, G-CSF decreases the rate of abortion in RSA mice and may provide some assistance in the treatment of patients with RSA.

scholarly journals G-CSF: One of The Vehicles for Communication Between Trophoblasts and Macrophages, Which May Cause Problems in Recurrent Spontaneous Abortion

2021 ◽  
Author(s):  
Peng Gao ◽  
Haiyi Liu ◽  
Ying Zha ◽  
Lijie Wei ◽  
Xuan Zhou ◽  
...  
Keyword(s):  
Spontaneous Abortion ◽  
Macrophage Activation ◽  
Cell Activity ◽  
Cell Communication ◽  
Recurrent Spontaneous Abortion ◽  
Granulocyte Colony Stimulating Factor ◽  
Pregnancy Failure ◽  
Normal Tissues ◽  
Key Factor ◽  
Stimulating Factor

Abstract Background The etiology of about half of the patients with recurrent spontaneous abortion (RSA) remains unclear, and the imbalance of the immune inflammatory response at the mother-foetal interface may be one of the keys to the onset. Granulocyte-colony stimulating factor (G-CSF) is thought to have a protective effect on pregnancy, and its absence may lead to pregnancy failure, but the evidence is scant. This study aims at investigating whether the loss of G-CSF induced RSA by affecting cell communication at the maternal-foetal interface. Results G-CSF was mainly expressed in villus rather than decidua, and the expression in RSA tissues was lower than that in normal tissues. Down-regulation of G-CSF in trophoblasts resulted in decreased cell activity. Trophoblast-derived exosomes inhibited macrophage activation, while G-CSF free exosomes did not. Intraperitoneal injection of G-CSF improved the pregnancy outcome of RSA mice, and the expression of G-CSF and its receptor at the mother-foetal interface also changed. Conclusion The expression of G-CSF was found to be decreased in villi of patients with RSA. The absence of G-CSF weakens the immune suppression of trophoblasts against macrophages, and the function of trophoblasts is impaired, which may be a key factor in the occurrence of RSA. G-CSF decreased the rate of abortion in RSA mice, and might provide some assistance in the treatment of patients with RSA.

Use of granulocyte-colony stimulating factor as adjuvant therapy in patients with recurrent pregnancy failure

2016 ◽  
Vol 115 ◽  
pp. 69 ◽  
Author(s):  
Juana Gil-Herrera ◽  
Jose Luis Vicario ◽  
Alberto Garcia-Enguídanos ◽  
Esther Marbán ◽  
Vanesa de Lucas ◽  
...  
Keyword(s):  
Adjuvant Therapy ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Pregnancy Failure ◽  
Stimulating Factor

scholarly journals Inhibition of Macrophage Activation by the Myxoma Virus M141 Protein (vCD200)

2009 ◽  
Vol 83 (18) ◽  
pp. 9602-9607 ◽  
Author(s):  
Leiliang Zhang ◽  
Marianne Stanford ◽  
Jia Liu ◽  
Catherine Barrett ◽  
Lei Jiang ◽  
...  
Keyword(s):  
Macrophage Activation ◽  
Myxoma Virus ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Granulocyte Colony Stimulating Factor ◽  
Wild Type ◽  
Protein Levels ◽  
Rapid Activation ◽  
Stimulating Factor ◽  
Necrosis Factor

ABSTRACT The M141 protein of myxoma virus (MYXV) is a viral CD200 homolog (also called vOX-2) that inhibits macrophage activation in infected rabbits. Here, we show that murine myeloid RAW 264.7 cells became activated when infected with MYXV in which the M141 gene was deleted (vMyx-M141KO) but not with the parental wild-type MYXV. Moreover, transcript and protein levels of tumor necrosis factor and granulocyte colony-stimulating factor were rapidly upregulated in an NF-κB-dependent fashion in the RAW 264.7 cells infected with vMyx-M141KO. M141 protein is present in the virion and counteracts this NF-κB activation pathway upon infection with the wild-type MYXV. Our data suggest that upregulation of these classic macrophage-related proinflammatory cytokine markers following infection of myeloid cells with the M141-knockout MYXV is mediated via the rapid activation of the cellular NF-κB pathway.

Use of Granulocyte-Colony Stimulating Factor as adjuvant therapy in patients with recurrent pregnancy failure

2016 ◽  
Vol 115 ◽  
pp. 30 ◽  
Author(s):  
Juana Gil-Herrera ◽  
Jose Luis Vicario ◽  
Alberto Garcia-Enguídanos ◽  
Esther Marbán ◽  
Vanesa de Lucas ◽  
...  
Keyword(s):  
Adjuvant Therapy ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Pregnancy Failure ◽  
Stimulating Factor
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