Placental inflammation, lifestyle, maternal and early child sensitisation to allergens - the assessment of lifestyle and allergic disease during infancy birth cohort.

AIM: To investigate (i) whether maternal sensitisation to allergens, and lifestyle can influence the risk of acute and chronic inflammation of the placenta, in the forms of chorioamnionitis and villitis, respectively, and (ii) whether these placental inflammations are associated with the outcome of sensitisation for the child during preschool age. METHODS: Placentas from term uncomplicated pregnancies (n = 275) in the assessment of lifestyle and allergic disease during infancy study were analysed for the presence of acute chorioamnionitis and chronic villitis. Stepwise logistic regression was performed to estimate the relative risk of placental inflammation in relation to maternal allergic sensitisation and lifestyle, and the association between placental inflammation and sensitisation of the child up to five years of age. RESULTS: Parity and delivery at home were independently associated with chorioamnionitis, home delivery only with the low grade. Maternal allergic sensitisation was associated with increased risk of villitis in the bivariable model, however, not in the multivariable model. No significant associations were detected between placental inflammation and the outcome of sensitisation to allergens at five years of age. CONCLUSION: Our data do not support the hypothesis that the increased risk for sensitisation of a child when the mother is allergic is mediated via placental inflammation.

Mechanisms of IgE-mediated allergy.

Allergic diseases are a global health problem today. Knowledge is still lacking about what causes some people to develop allergies while others remain tolerant to environmental antigens. The recent increase in prevalence suggests an involvement of gene-environment interactions and epigenetic mechanisms. Since allergies often develop early in life, the intrauterine environment has been proposed to play a role in predisposing some individuals to become allergic. The development of techniques to produce allergens as highly pure recombinant proteins has improved the tools for allergy diagnosis and treatment. Novel strategies for allergen-specific immunotherapy include tailor-made vaccines and alternative routes for administration.

The number of CD68(+) (Hofbauer) cells is decreased in placentas with chorioamnionitis and with advancing gestational age.

Hofbauer cells are placental macrophages found in chorionic villous stroma; they express classic monocyte/macrophage markers, such as CD68. Little is known about their participation in placental disease and immunologic interactions at the placental interface. The aim of this study was to quantify the amount of Hofbauer cells in placentas complicated, or not, by chorioamnionitis and in placentas from different gestational ages. Fifty-eight 2nd- and 3rd-trimester placentas with the histologic diagnosis of acute chorioamnionitis were compared with 42 control placentas matched according to gestational age. Immunohistochemistry evaluation was performed with a monoclonal anti-CD68 antibody. Five areas of each placenta were photographed and 5 investigators, with the help of a computerized image analysis program, independently evaluated the number of CD68(+) cells. Our results showed that there are significantly fewer CD68(+) cells per villous area in placentas diagnosed with chorioamnionitis than in those of controls (P < 0.001). Moreover, there was a significant overall decrease in the number of these cells in 3rd as compared with 2nd trimester placentas (P  =  0.02), as well as in placentas from term as compared to preterm pregnancies (P  =  0.004). Our data indicate that CD68(+) Hofbauer cells may be involved in placental infection and possibly associated with the developmental maturation of the fetoplacental unit.

Toll-like receptor-2 expression in normal and pathologic human placenta.

Toll-like receptors (TLRs) are important components of the innate immune system and are expressed by trophoblast in normal full-term placenta. At present, not much is known about the role of TLRs during normal pregnancy and in pregnancy complicated by infection. In this study, we have used immunohistochemistry to investigate the expression of TLR2 in 58 placentas from second and third trimester with chorioamnionitis and 25 full-term placentas from uncomplicated pregnancies without chorioamnionitis. TLR2 was found to be localized to the cyto- and syncytio-trophoblast cell layer and to decidual stromal cells. The expression of TLR2 in placentas with chorioamnionitis was significantly lower than in placentas without chorioamnionitis. Furthermore, there was a significantly higher expression in placentas from liveborn children than in placentas from stillborn/aborted fetuses and also a higher expression in second- than in third-trimester placentas. These data suggest that TLR2 expression in the trophoblast could be involved in the response to infectious pathogens in the placenta.