Another important population of cells found in the bovine placenta are the fetal macrophages. These cells are referred to in human medicine as ‘‘Hofbauer Cells’’
Ž .
Benirschke and Kaufmann, 1995 . Fetal placental macrophages may originate either from chorionic mesenchyme early in gestation, or from fetal bone marrow-derived
monocytes. These cells produce pro-inflammatory cytokines and function in antigen presentation suggesting that they can function as sentinel cells, are important in fetal
defense and may contribute to transplacental transmission of microbial agents.
5. Disease states
In twinning during bovine pregnancy, placental vessels nearly always fuse. The establishment of shared vasculatures results in fetal chimarism. In male–female twin
pairs, this causes characteristic, marked changes in development of the gonads, and internal tubular and external genitalia of the female fetus and is recognized as ‘‘free-
martinism’’.
Placentation is important in understanding the pathogenesis of some congenital diseases, mechanisms of transplacental transmission of teratogenic microbial agents, and
Ž .
failure of pregnancy of cloned calves Hill et al., 1999 . It is beyond the scope of this review to address all aspects of in utero infection. Those infectious diseases that produce
grossly evident lesions are limited to chronic fungal and bacterial infections. Mycotic infections, most commonly, Aspergillus sp., cause chronic placentitis with severe
Ž .
necrosis and destruction of cotyledonary villi. Brucellosis and yeast infection Candida also result in chronic infection with ‘‘functional amputation’’ of cotyledonary tissues
leading to either in utero growth retardation, severe fetal distress, and commonly, Ž
. abortion Anderson et al., 1986; Foley and Schlafer, 1987 . Transplacental transmission
of most viral agents occurs with no grossly evident tissue destruction. The most common disease of the bovine placenta is placental retention. The precise
mechanisms that are triggered, and lead to placental release are not understood. Failure Ž
. of placental release is common values cited range from 3 to 12 and is higher in
individual animals that abort or calve prematurely, in cases of twinning, following Ž
. induced deliveries, etc.
see review by Laven and Peters, 1996 . During normal maturation prior to delivery, binucleate trophoblast numbers decrease dramatically but
Ž this change does not occur in placentas that are retained Gross et al., 1991; Williams et
. al., 1987 . The mechanisms for this are not known.
Field studies have demonstrated an association between the major histocompatibility Ž
. complex MHC Class I compatibility of a dam and her fetus with placental retention
Ž .
Joosten et al., 1991; Joosten and Hensen, 1992 . In cases where dam and fetus share MHC Class I antigens, placental retention is more likely to occur. This suggests a
central role for histocompatibility in triggering an immune reaction that contributes to placental release. Class I antigens have been detected on trophoblast cells in the
Ž .
Ž .
intercotyledonary area Low et al., 1990 . Davies et al. 2000 have recently expanded this observation by showing that during normal pregnancy, MHC Class I is expressed by
trophoblast cells in the intercotyledonary areas and in the arcade area of the placentome from the 6th month of gestation.
6. Placental macrophages: ontogeny during bovine pregnancy
