Pre-eclampsia affects procalcitonin production in placental tissue

Chiara Agostinis, Damiano Rami, Paola Zacchi, Fleur Bossi, Tamara Stampalija, Alessandro Mangogna, Leonardo Amadio, Romana Vidergar, Liza Vecchi Brumatti, Giuseppe Ricci, Claudio Celeghini, Oriano Radillo, Ian Sargent, Roberta Bulla

Research output: Contribution to journalArticle

Abstract

Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.

Original languageEnglish
Article numbere12823
JournalAmerican Journal of Reproductive Immunology
Volume79
Issue number4
DOIs
Publication statusPublished - Apr 1 2018

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Calcitonin
Pre-Eclampsia
Placenta
Serum
Macrophages
Trophoblasts
Up-Regulation
Neuroendocrine Cells
Monocytes
Anti-Idiotypic Antibodies
Thyroid Gland

Keywords

  • adalimumab
  • calcitonin gene-related peptide
  • placenta
  • pre-eclampsia
  • procalcitonin

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Reproductive Medicine
  • Obstetrics and Gynaecology

Cite this

Pre-eclampsia affects procalcitonin production in placental tissue. / Agostinis, Chiara; Rami, Damiano; Zacchi, Paola; Bossi, Fleur; Stampalija, Tamara; Mangogna, Alessandro; Amadio, Leonardo; Vidergar, Romana; Vecchi Brumatti, Liza; Ricci, Giuseppe; Celeghini, Claudio; Radillo, Oriano; Sargent, Ian; Bulla, Roberta.

In: American Journal of Reproductive Immunology, Vol. 79, No. 4, e12823, 01.04.2018.

Research output: Contribution to journalArticle

Agostinis, C, Rami, D, Zacchi, P, Bossi, F, Stampalija, T, Mangogna, A, Amadio, L, Vidergar, R, Vecchi Brumatti, L, Ricci, G, Celeghini, C, Radillo, O, Sargent, I & Bulla, R 2018, 'Pre-eclampsia affects procalcitonin production in placental tissue', American Journal of Reproductive Immunology, vol. 79, no. 4, e12823. https://doi.org/10.1111/aji.12823
Agostinis, Chiara ; Rami, Damiano ; Zacchi, Paola ; Bossi, Fleur ; Stampalija, Tamara ; Mangogna, Alessandro ; Amadio, Leonardo ; Vidergar, Romana ; Vecchi Brumatti, Liza ; Ricci, Giuseppe ; Celeghini, Claudio ; Radillo, Oriano ; Sargent, Ian ; Bulla, Roberta. / Pre-eclampsia affects procalcitonin production in placental tissue. In: American Journal of Reproductive Immunology. 2018 ; Vol. 79, No. 4.
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abstract = "Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.",
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AU - Agostinis, Chiara

AU - Rami, Damiano

AU - Zacchi, Paola

AU - Bossi, Fleur

AU - Stampalija, Tamara

AU - Mangogna, Alessandro

AU - Amadio, Leonardo

AU - Vidergar, Romana

AU - Vecchi Brumatti, Liza

AU - Ricci, Giuseppe

AU - Celeghini, Claudio

AU - Radillo, Oriano

AU - Sargent, Ian

AU - Bulla, Roberta

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Y1 - 2018/4/1

N2 - Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.

AB - Problem: Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions. Method: Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed. Results: Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera. Conclusion: Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.

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