The Structure of the Human Placenta: Implications for Initiating and Defending Against Virus Infections

Abstract

The architecture of the human placenta permits an extensive and intimate association between the maternal and fetal circulations. The fetal component consists of the elaborately branched villous tree, and this is bathed directly by maternal blood circulating within the intervillous space. Whilst this arrangement may favour metabolic exchange, it poses considerable risks for the vertical transmission of pathogens. Some features of placental structure can be considered potential impediments to transmission, such as the syncytial nature of the outer villous covering, the syncytiotrophoblast, and the ability of this tissue to secrete both nitric oxide and interferons. Other features may facilitate vertical transmission, including the lack of expression of MHC Class 1 antigens by the syncytiotrophoblast, and its vesicular and immunoglobulin transport pathways. More importantly, it is known that physical defects occur in the trophoblast layers at all stages in gestation. Whilst repair processes have been identified it must be assumed that pathogens or infected maternal white cells have access to the trophoblastic basement membrane, albeit transiently. The universal nature of these defects suggests that the trophoblast cannot be of paramount importance in the prevention of transmission. Rather, the defence mechanisms must lie either at the level of the basement membrane or within the villous core. There they may be represented by the resident macrophage population or the capillary endothelial cells and their junctional complexes. Consequently, the placenta should be viewed as an active rather than a passive barrier. © 1997 by John Wiley & Sons, Ltd.

Adhesion of Toxoplasma gondii tachyzoite-infected vehicle leukocytes to capillary endothelial cells triggers timely parasite egression

“…It had been thought that extravasation of these infected leukocytes transfers the microorganisms from the blood to solid organs beyond the blood vessel wall, in a “Trojan horse”-like manner 23–25 . However, several intracellular microorganisms are reported to invade the brain and placenta 24, 26–28 , where migration of leukocytes out of the blood vessels is barely detectable 29, 30 . Furthermore, it was recently reported that T .…”

A critical assessment of the “sterile womb” and “in utero colonization” hypotheses: implications for research on the pioneer infant microbiome

“…Because the placenta is generally considered a barrier to protect the fetus from microbial pathogens that invade the blood stream of the mother [32, 33], studies directly aimed at the determination of a “placental microbiome” in healthy pregnancies are scarce. Instead, microbial studies were, for the most part, focused on complications of pregnancy or the birth process, such as spontaneous abortions (21 and 24% positive aerobic and anaerobic cultures, respectively; n  = 47) [34], or suspected or confirmed cases of infant infection (33% positive cases, n  = 33 and 32% positive cases, n  = 72, as reported by [35, 36], respectively).…”

Placenta-on-a-chip: a novel platform to study the biology of the human placenta

“…Its most important function is the exchange of endogenous and exogenous substances, which enables adequate supply of oxygen and nutrients, excretion of fetal metabolic waste (1–6), and protection against potentially harmful agents, such as xenobiotics (7–11), bacteria (12–17), viruses (18–26), and parasites (26–32). Transfer of substances between the intervillous space and fetal capillaries takes place across a multilayered structure often called the “placental barrier,” which is composed of trophoblasts, connective tissue, basal lamina, and the fetal endothelium (1–6, 33–37).…”