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Abstract
Preeclampsia (PE) is defined as a hypertensive and coagulative disorder affecting about 2–8% of all pregnancies and is one of the main causes of maternal and fetal morbidity and mortality. Despite the great amount of studies run in this field, little is known about the precise pathogenic mechanisms behind PE. While endothelial and trophoblast dysfunctions, exaggerated inflammatory response, and hypercoagulative state have been shown to play a key role in the occurrence of PE, the primary trigger is still unknown. One of the hypotheses is that some infectious agents may represent a trigger for PE onset. Consistently, higher seroprevalence of Helicobacter pylori (HP) infection, a Gram-negative bacterium with a specific tropism for human gastric mucosa, has been shown in women with PE. Even tighter association has been found between PE and infection with cytotoxin-associated gene-A (CagA)-positive strains of HP. Recent in vitro studies have shown that anti-CagA antibodies cross-react with human trophoblast cells and determine a functional impairment in terms of cell invasiveness, thus, providing the first pathogenic model of HP infection-mediated placental damage. Since in the early process of implantation and placental development, trophoblast invasion of maternal decidua is a crucial step, the proposed autoimmune mechanism induced by HP infection, negatively interfering with the fetal side of the early developing placenta, may represent a mechanism explaining the higher seropositivity for HP infection among PE women. However, the contribution of HP infection to the pathogenesis of PE or to the worsening of its clinical presentation need to be further investigated as well as the possible impact of pre-pregnancy screening and eradication of HP infection on the incidence of the syndrome.
Highlights
Pre eclampsia (PE) is generally defined as new hypertension and substantial proteinuria at or after 20 weeks’ gestation [1]
ANTI-cytotoxinassociated gene-A (CagA) ANTIBODIES CLASS IgG-MEDIATED TROPHOBLAST INVASION INHIBITION: AN IN VITRO MODEL OF Helicobacter pylori (HP)-INDUCED POOR PLACENTATION To try to answer that question, we investigated whether HP infection might induce an immune humoral response able to trigger an autoantibody-mediated placental cellular damage
To better understand the molecular mechanisms involved in the antibody-mediated functional impairment of trophoblast cells, we examined the effect of anti-CagA on ERK activation and NF-kB nuclear translocation, two important factors activated during trophoblast proliferation, and we observed that anti-CagA antibodies are able to inhibit the activation of both elements [24]
Summary
Pre eclampsia (PE) is generally defined as new hypertension and substantial proteinuria at or after 20 weeks’ gestation [1]. A dysfunctional and hypoxic placenta is considered to release factors into the maternal circulation that cause the clinical features of this condition, including hypertension and proteinuria, as well as clotting and liver dysfunction These appear to arise from a generalized systemic inflammatory response, of which endothelial dysfunction is a prominent component [7]. To better understand the molecular mechanisms involved in the antibody-mediated functional impairment of trophoblast cells, we examined the effect of anti-CagA on ERK activation and NF-kB nuclear translocation, two important factors activated during trophoblast proliferation, and we observed that anti-CagA antibodies are able to inhibit the activation of both elements [24] As a whole, these observations provided a possible autoimmune pathogenic mechanism induced by HP infection, negatively interfering with the fetal side of placental development. This pathogenic model of autoimmune-mediated placental impairment is the first one linking HP infection, poor placentation, and PE (Figure 1)
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