Altered monocyte function in experimental preeclampsia in the rat

Faas, Marijke M.; Broekema, Martine; Moes, Hendrik; Schaaf, Gerda van der; Heineman, Maas Jan; Vos, Paul de

doi:10.1016/j.ajog.2004.03.041

Cited by 43 publications

(29 citation statements)

References 22 publications

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“…TNF-α may cause indirect trophoblastic cell damage through its effects on differentiation of lymphokine-activated killer cells (Clark, 1998). The higher levels of TNF-α and IL-1β and their positive correlation with well-established parameters of pregnancy toxaemia including serum uric acid and proteinuria in the present study equally suggest that such cytokines are also mediators of placental inflammation and pathologies and subsequent systemic inflammatory reactions in ewe pregnancy toxaemia, as they have been previously been implicated in pregnancy toxemia in women and laboratory animals (Wang and Walsh, 1996;Faas et al, 2004).…”

Section: Discussionsupporting

confidence: 73%

Elevated Plasma Levels of Interleukin 1β, Tumour Necrosis Factor α and Monocyte Chemotactic Protein 1 Are Associated with Pregnancy Toxaemia in Ewes

2007

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Pregnancy toxaemia is a metabolic disorder that results from an inadequate energy supply to the growing maternal-fetal unit. The mechanism underlying the pathogenesis of the syndrome has not been fully clarified; however, a key role for cytokines and chemokines including interleukin 1 beta (IL-1 beta), tumour necrosis factor alpha (TNF-alpha) and monocyte chemotactic protein 1 (MCP-1) has been indicated in women and experimental animals. However, information on the maternal plasma levels of IL-1 beta, TNF-alpha and MCP-1 in ewes with pregnancy toxaemia is limited. Thus, the present study was designed to determine plasma IL-1 beta, TNF-alpha and MCP-1 concentrations in ewes with severe (n=6) and mild (n=4) naturally occurring pregnancy toxaemia and in uncomplicated pregnant ewes (n=10) using enzyme-linked immunosorbent assay (ELISA). All ewes with pregnancy toxaemia had significantly lower body temperature and respiratory rate than uncomplicated pregnant ewes (p<0.05). With the highest concentrations in severe cases, heart rate, proteinuria and serum uric acid levels as well as plasma IL-1 beta, TNF-alpha and MCP-1 were significantly different among all three groups (p<0.05). The plasma concentrations of IL-1 beta in control ewes and ewes with mild and severe toxaemia were 15.81 +/- 3.90 pg/ml, 23.83 +/- 2.42 pg/ml and 34.55 +/- 8.03 pg/ml, respectively. The plasma concentrations of TNF-alpha in control ewes and ewes with mild and severe toxaemia were 7.71 +/- 1.61 pg/ml, 16.13 +/- 3.63 pg/ml, and 22.85 +/- 3.64 pg/ml, respectively. The plasma concentrations of MCP-1 in control ewes and ewes with mild and severe toxaemia were 101.70 +/- 9.86 pg/ml, 134.75 +/- 6.24 pg/ml, and 157.67 +/- 9.69 pg/ml, respectively. Moreover, plasma IL-1 beta, TNF-alpha and MCP-1 levels were positively correlated with clinical and well-establish biochemical parameters of pregnancy toxaemia, serum uric acid and proteinuria (p<0.01). Concomitant increase of plasma IL-1 beta, TNF-alpha and MCP-1 concentrations along with serum uric acid, proteinuria, and worsening of the clinical signs indicates that such cytokines are involved in the aetiopathogenesis and in perpetuation of the local and systemic inflammatory reactions in pregnancy toxaemia in ewes. Hence, plasma IL-1 beta, TNF-alpha and MCP-1 may potentially serve as markers to monitor prognosis of pregnancy toxaemia in ewes.

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Section: Discussionsupporting

confidence: 73%

Elevated Plasma Levels of Interleukin 1β, Tumour Necrosis Factor α and Monocyte Chemotactic Protein 1 Are Associated with Pregnancy Toxaemia in Ewes

2007

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“…Our study identified that an average of 11% of the leukocytes were monocytes in the periphery of the laboratory rats, versus about 20% in the wild rats (Table 4). A review of the literature corroborates the observation that the levels of monocytes in laboratory rats is relatively low, estimated to be 0 to 5% [3], 2-3% [21], and 10% [27] of the total leukocytes, depending on the study. Thus, the literature is consistent with the idea that laboratory rats have lower levels of peripheral monocytes than do the wild rats used in this study.…”

Section: Monocytes and Granulocytes In The Periphery And Spleen Of Wisupporting

confidence: 65%

Immune Characterization of Wild-CaughtRattus norvegicusSuggests Diversity of Immune Activity in Biome-Normal Environments

Lin¹,

Holzknecht²,

Trama³

et al. 2012

Journal of Evolutionary Medicine

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Biome depletion, or loss of co-evolved constituents within the ecosystem of the human body, has become the leading suspect in epidemics of allergic, inflammatory and autoimmune diseases associated with post-industrial culture. Immunity in wild and laboratory rats has been used as a model for immunity in biomenormal and biome depleted environments, respectively. In this study, the ranges of numerous immune parameters (such as cytokine production and cell surface marker expression) in 8 wild rats overlapped with the ranges found in 7 laboratory rats. However, considering a number of parameters simultaneously as an "expression index" revealed a substantially greater range of immune activity in the wild compared with laboratory rats. These findings are consistent with the intuitive idea that the immune system is inherently malleable or flexible within environments of evolutionary adaptedness, and might suggest that biome reconstitution as an effective therapy could be achieved in a variety of ways.

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“…*P < 0.05, **P < 0.01. [28][29][30]. Inspired by this model, we tested the hypothesis that CD81 overproduction participates in preeclamptic placentation and triggers the clinical manifestations of PE.…”

Section: Cd81-induced Rat Model Mimics the Phenotype Of Human Pementioning

confidence: 99%

Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

Shen

Diao

Sun

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Preeclampsia (PE) is initiated by abnormal placentation in the early stages of pregnancy, followed by systemic activation of endothelial cells of the maternal small arterioles in the late second or third trimester (TM) of pregnancy. During normal pregnancy, placental cytotrophoblasts (CTBs) invade the maternal uterine wall and spiral arteries, whereas this process is interrupted in PE. However, it is not known how the malformed placenta triggers maternal endothelial crisis and the associated manifestations. Here, we have focused on the association of CD81 with PE. CD81, a member of the tetraspanin superfamily, plays significant roles in cell growth, adhesion, and motility. The function of CD81 in human placentation and its association with pregnancy complications are currently unknown. In the present study, we have demonstrated that CD81 was preferentially expressed in normal first TM placentas and progressively downregulated with gestation advance. In patients with early-onset severe PE (sPE), CD81 expression was significantly up-regulated in syncytiotrophoblasts (STBs), CTBs and the cells in the villous core. In addition, high levels of CD81 were observed in the maternal sera of patients with sPE. Overexpressing CD81 in CTBs significantly decreased CTB invasion, and culturing primary human umbilical vein endothelial cells (HUVECs) in the presence of a high dose of exogenous CD81 resulted in interrupted angiogenesis and endothelial cell activation in vitro. Importantly, the phenotype of human PE was mimicked in the CD81-induced rat model.is characterized by a new onset of hypertension and proteinuria after 20 wk of gestation. Early-onset severe PE (sPE, ≤ 34 wk) is associated with a high incidence of eclampsia, cerebrovascular complications, and fetal growth restriction, which severely threaten maternal and fetal health (1). Although the etiology of PE remains elusive, this disease has two known stages: In stage I, inadequate cytotrophoblast (CTB) invasion early in the pregnancy causes abnormal placentation; in stage II, systemic endothelial cell activation and clinical manifestations occur in the second or third trimester (TM), which are associated with the release of molecules and factors from the shallowly implanted placenta (2, 3).CD81 is a widely expressed tetraspanin that provides a scaffold for signaling molecules and orchestrates interactions between membrane-associated proteins to initiate signaling cascades that regulate cell adhesion, migration, and invasion (4-7). CD81 is also a tumor suppressor that inhibits the migration and invasion of some malignant tumor cells (8, 9). In addition, an increasing number of studies have reported that CD81 is one of the main components of exosomes and can be released into maternal circulation or delivered to certain organs and tissues (10-12). Our previous study showed that CD81 is highly expressed in LPS-treated HTR-8/SV neo cells derived from human first TM extravillous trophoblast cells and induces trophoblast syncytialization (13); however, the role of CD81 in ...

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Altered monocyte function in experimental preeclampsia in the rat

Cited by 43 publications

References 22 publications

Elevated Plasma Levels of Interleukin 1β, Tumour Necrosis Factor α and Monocyte Chemotactic Protein 1 Are Associated with Pregnancy Toxaemia in Ewes

Elevated Plasma Levels of Interleukin 1β, Tumour Necrosis Factor α and Monocyte Chemotactic Protein 1 Are Associated with Pregnancy Toxaemia in Ewes

Immune Characterization of Wild-CaughtRattus norvegicusSuggests Diversity of Immune Activity in Biome-Normal Environments

Up-regulation of CD81 inhibits cytotrophoblast invasion and mediates maternal endothelial cell dysfunction in preeclampsia

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