Perfusion of human term placentas with lipopolysaccharide did not affect the capacity of the fetal and maternal tissues to produce interleukin-10

Mahmoud Huleihel, Amash Alaa, Sapir Olga, E. Maor, Sharon Levy, Miriam Katz, Leslie Myatt, Holcberg Gershon

Research output: Contribution to journalArticle

3 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)229-233
Number of pages5
JournalEuropean Cytokine Network
Volume14
Issue number4
StatePublished - Oct 2003
Externally publishedYes

Fingerprint

Interleukin-10
Placenta
Lipopolysaccharides
Fetus
Perfusion
Mothers
Tissue
Chorion
Amnion
Decidua
Macrophages
Trophoblasts
Fibroblasts
Anti-Inflammatory Agents
Down-Regulation
Epithelial Cells
Enzyme-Linked Immunosorbent Assay
Cells
Staining and Labeling
Cytokines

Keywords

  • Amnion
  • Chorion
  • IL-10
  • Lipopolysaccharide
  • Term delivery
  • Trophoblasts

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

Cite this

Perfusion of human term placentas with lipopolysaccharide did not affect the capacity of the fetal and maternal tissues to produce interleukin-10. / Huleihel, Mahmoud; Alaa, Amash; Olga, Sapir; Maor, E.; Levy, Sharon; Katz, Miriam; Myatt, Leslie; Gershon, Holcberg.

In: European Cytokine Network, Vol. 14, No. 4, 10.2003, p. 229-233.

Research output: Contribution to journalArticle

Huleihel, Mahmoud ; Alaa, Amash ; Olga, Sapir ; Maor, E. ; Levy, Sharon ; Katz, Miriam ; Myatt, Leslie ; Gershon, Holcberg. / Perfusion of human term placentas with lipopolysaccharide did not affect the capacity of the fetal and maternal tissues to produce interleukin-10. In: European Cytokine Network. 2003 ; Vol. 14, No. 4. pp. 229-233.
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T1 - Perfusion of human term placentas with lipopolysaccharide did not affect the capacity of the fetal and maternal tissues to produce interleukin-10

AU - Huleihel, Mahmoud

AU - Alaa, Amash

AU - Olga, Sapir

AU - Maor, E.

AU - Levy, Sharon

AU - Katz, Miriam

AU - Myatt, Leslie

AU - Gershon, Holcberg

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N2 - 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.

AB - 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.

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