@Article{,
AUTHOR = {Mahmoud Huleihel, Amash Alaa, Sapir Olga, Maor E, Sharon Levy, Miriam Katz, Lesly Myatt, Holcberg Gershon},
TITLE = {Perfusion of human term placentas with lipopolysaccharide did not affect the capacity of the fetal and maternal tissues to produce interleukin-10},
JOURNAL = {European Cytokine Network},
VOLUME = {14},
YEAR = {2003},
NUMBER = {4},
PAGES = {229--233},
URL = {http://www.techscience.com/ECN/v14n4/66520},
ISSN = {1952-4005},
ABSTRACT = {IL-10 is anti-inflammatory cytokine that is involved in the regulation of the pregnancy process. We
examined the capacity of fetal and maternal placental tissues from human term placentas, to produce IL-10, in
the presence and absence of LPS. The levels of IL-10 were examined (by ELISA and immunohistochemical
staining) in the fetal and maternal tissues of human placentas after 10 hours of perfusion, in the presence or
absence of lipopolysaccharide (LPS; 1 µg/k”g perfused tissue). We could detect IL-10 in amnion (A;
13.91 ± 11.35 pg/ml) and chorion (CH; 7.85 ± 6.38 pg/ml) tissue homogenates, and in the homogenates of three
different sites of the placental tissue compartment (subchorionic placenta (SubCH); 7.39 ± 4.39 pg/ml, mid-placenta
(MidPL); 8.9 ± 4.73 pg/ml and decidua (Decid); 16.48 + 11.86 pg/ml). Immunohistochemical studies
showed that IL-10 was localized in the epithelial cells of the amnion, and in the fibroblasts and macrophages of
the chorion. In the placenta and mid-placental sites, IL-10 is localized mainly in cytotrophoblasts and
syncytotrophoblasts. The presence of LPS in the perfusion media of the placentas for 10 hours, did not
significantly affect the capacity of the fetal and maternal tissues to produce IL-10. Thus, our results may indicate
the involvement of the fetal compartment in the down-regulation of the cell-mediated response of the maternal
compartment against the fetus, by producing IL-10 under physiological conditions. Infection/inflammation agents
such as LPS did not affect the expression levels of IL-10 in the placenta},
DOI = {}
}