Comparative phenotypic characterization of human cord blood monocytes and placental macrophages at term

Selkov, S. A.; Selutin, A.V.; Pavlova, Oksana; Khromov-Borisov, N. N.; Павлов, О. В.

doi:10.1016/j.placenta.2013.05.007

Cited by 16 publications

(14 citation statements)

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“…In wounds, virtually every type of immune cell appears, producing cytokines and growth factors that support the healing process. Increased cytokine expression does not only happen after trauma or infection, but also in physiologic states including pregnancy and other situations where increased cell proliferation and matrix deposition are required …”

Section: The Pathophysiology Underlying Hypoalbuminemiamentioning

confidence: 99%

“…Increased cytokine expression does not only happen after trauma or infection, but also in physiologic states including pregnancy and other situations where increased cell proliferation and matrix deposition are required. [8][9][10] In acute wounds or infected areas, repair is stimulated by proinflammatory and inflammatory cytokines, and visible wound edema occurs due to expansion of the interstitial space ( Figure 1). Both phases of cytokine and growth factor expression support different inflammatory processes.…”

Section: Inflammation Increased Capillary Permeability and Hypoalbumentioning

confidence: 99%

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Hypoalbuminemia: Pathogenesis and Clinical Significance

Soeters

Wolfe

Shenkin

2018

J Parenter Enteral Nutr

758

554

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Hypoalbuminemia is associated with inflammation. Despite being addressed repeatedly in the literature, there is still confusion regarding its pathogenesis and clinical significance. Inflammation increases capillary permeability and escape of serum albumin, leading to expansion of interstitial space and increasing the distribution volume of albumin. The half‐life of albumin has been shown to shorten, decreasing total albumin mass. These 2 factors lead to hypoalbuminemia despite increased fractional synthesis rates in plasma. Hypoalbuminemia, therefore, results from and reflects the inflammatory state, which interferes with adequate responses to events like surgery or chemotherapy, and is associated with poor quality of life and reduced longevity. Increasing or decreasing serum albumin levels are adequate indicators, respectively, of improvement or deterioration of the clinical state. In the interstitium, albumin acts as the main extracellular scavenger, antioxidative agent, and as supplier of amino acids for cell and matrix synthesis. Albumin infusion has not been shown to diminish fluid requirements, infection rates, and mortality in the intensive care unit, which may imply that there is no body deficit or that the quality of albumin “from the shelf” is unsuitable to play scavenging and antioxidative roles. Management of hypoalbuminaemia should be based on correcting the causes of ongoing inflammation rather than infusion of albumin. After the age of 30 years, muscle mass and function slowly decrease, but this loss is accelerated by comorbidity and associated with decreasing serum albumin levels. Nutrition support cannot fully prevent, but slows down, this chain of events, especially when combined with physical exercise.

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Section: The Pathophysiology Underlying Hypoalbuminemiamentioning

confidence: 99%

Section: Inflammation Increased Capillary Permeability and Hypoalbumentioning

confidence: 99%

Hypoalbuminemia: Pathogenesis and Clinical Significance

Soeters

Wolfe

Shenkin

2018

J Parenter Enteral Nutr

758

554

View full text Add to dashboard Cite

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“…Throughout the first trimester of pregnancy they arise from mesenchymal progenitor cells (14); in the second and third trimester, it is suspected that monocytes are recruited from the fetal circulation and differentiate to HBCs within the placenta (15, 16). HBCs are assumed to move through the placental stroma toward sites where they are needed (17).…”

Section: Introductionmentioning

confidence: 99%

Human Placental Hofbauer Cells Maintain an Anti-inflammatory M2 Phenotype despite the Presence of Gestational Diabetes Mellitus

et al. 2017

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BackgroundHofbauer cells (HBCs) are macrophages of the feto-placental unit. Despite the general view that these cells have an anti-inflammatory M2 phenotype, recent studies have claimed that pregnancy pathologies—e.g., gestational diabetes mellitus (GDM)—cause a switch from an M2 to an M1 pro-inflammatory phenotype in HBCs. The pilot-study presented here challenges this claim, showing that HBCs maintain anti-inflammatory properties in spite of the hyperglycemic, low-grade inflammatory environment of GDM.MethodsHBCs were isolated from placentae of healthy women (N = 5) and women with GDM (N = 6) diagnosed in the second trimester. FACS was used to measure surface markers associated with either M1 or M2 phenotype on the cells. In addition, placental tissue sections were subjected to immune histochemical imaging to assess the phenotype within the tissue context. Supernatant from control and GDM HBCs was collected at defined time points and used in a multiplex ELISA-on-beads approach to assess secretion of cytokines, chemokines, and growth factors. The effect of HBC cell culture supernatant on placental endothelial activation was investigated.ResultsFACS and immune staining showed that, indeed, M2 markers, such as CD206 and CD209, are increased in HBCs isolated from GDM placentae. Also, the M1 marker CD86 was increased, but only by trend. Secretion of numerous cytokines, chemokines and growth factors was not changed; pro-inflammatory interleukin (IL)-1β and IL-6 release form GDM HBC was increased but not significant. Exposure to GDM HBC supernatant did not induce cell adhesion molecules (VCAM-1, selectins, vascular endothelial-cadherin) in placental endothelial cells compared to supernatant from control HBCs, an induction of intracellular adhesion molecule 1 was observed however.ConclusionOur study—although performed in a small set of patients—shows that placental macrophages maintain their anti-inflammatory, tissue remodeling M2 phenotype even in pregnancies affected by gestational diabetes. This consistent phenotype might be important for propagation of maternal tolerance toward the fetus and for protection of the fetus from a low-grade inflammatory environment.

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“…43 Our results of the comparative analysis of placental macrophages and cord blood monocytes were in accordance with these data and demonstrated a similar pattern of IL-17R expression in humans. 42 We believe that expression of IL-17R by the placental macrophages should be considered in the context of the conceivable gestational effects of IL-17. In in vitro experiments, IL-17 has been shown to activate macrophages and stimulate secretion of inflammatory cytokines.…”

Section: Mfi Indexmentioning

confidence: 99%

“…Our study provides convincing evidence of the ability of placental macrophages to produce IL-17A and IL-17F at early and late TA B L E 1 Intracellular expression of IL-17A and IL-17F in the placental macrophages no labour; L, with labour; nd, not determined; n, number of patients. This feature is one of the stark differences between populations of the placental macrophages and cord blood monocytes, with the latter being characterized by total IL-17R expression 42. This fact is of special significance, as other cell sources have not been unambiguously recognized so far in the foetal placenta; contradictory results have been obtained on the ability of cyto-and syncitiotrophoblasts to produce IL-17 22,23,27.…”

mentioning

confidence: 99%