title: Transport of maternal immunoglobulins through the human placental barrier in normal pregnancy and during inflammation.
abstract: We studied the effect of ascending infections of the birth canal on the transport of maternal immunoglobulins (Igs) through the placental barrier in humans. The study was performed on 41 human placentas obtained from embryos (n=21) and fetuses (n=20) who had died from different causes, including those connected with ascending infections of the birth canal, and seven placentas obtained after normal delivery at term. Different morphological and immunohistochemical methods were used. The transfer of Igs through the placental barrier is a complex process that involves tissues (trophoblast, stroma of the trophoblastic villi, and capillaries), cells (monocytes and erythroblasts) and molecular components (at least six types of transfer receptors and biologically active components). We found that the intensification of transfer of different types of maternal Igs (IgG, IgA, IgM) is accompanied by certain morphological and functional changes in the placental barrier. In normal development without infection, the transfer of IgG is steady and the process most intensive, while the transfer of IgA was evaluated in 75% of the cases, and of IgM in only 10%. Inflammation of the birth canal was accompanied by an increase in the transport of IgG in early embryogenesis, which was maintained throughout intrauterine development. In cases with moderate infection, transfer of IgG and IgA was found in all cases studied, while transfer of IgM was seen in 45% of the cases. In cases with massive infection, transfer of all three types of Igs was seen, the most intensive being of IgG and the least of IgM. Ascending infection of the birth canal changes dramatically the transport of Igs through the placenta and can be dangerous and even fatal for the embryo or fetus.
authors.affiliation: Laboratory of Experimental Medicine, Park Rabin, The Hebrew University of Jerusalem, Rehovot, Israel.
authors.forename: Herzl
authors.initials: H
authors.lastname: Ben-Hur
authors.forename: Pavel
authors.initials: P
authors.lastname: Gurevich
authors.forename: Asher
authors.initials: A
authors.lastname: Elhayany
authors.forename: Ilana
authors.initials: I
authors.lastname: Avinoach
authors.forename: David F
authors.initials: DF
authors.lastname: Schneider
authors.forename: Itshak
authors.initials: I
authors.lastname: Zusman
mesh_terms: D000208:Acute Disease; D015703:Antigens, CD / Q000032:analysis; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism; D007074:Immunoglobulin G / Q000378:metabolism; D007075:Immunoglobulin M / Q000378:metabolism; D007136:Immunoglobulins / Q000378:metabolism*; D007150:Immunohistochemistry; D007239:Infections / Q000378:metabolism / Q000503:physiopathology; D007249:Inflammation / Q000378:metabolism* / Q000503:physiopathology; D010920:Placenta / Q000098:blood supply / Q000737:chemistry / Q000378:metabolism*; D011247:Pregnancy; D021381:Protein Transport; D011961:Receptors, Fc / Q000032:analysis; D013997:Time Factors; D014327:Trophoblasts / Q000737:chemistry / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins; D011961:Receptors, Fc