Human amnion epithelial cells as a treatment for inflammation-induced fetal lung injury in sheep

Patricia Vosdoganes, Ryan Hodges, Rebecca Lim, Alana Westover, Rutu Acharya, Euan Wallace, Timothy Moss

Research output: Contribution to journalArticleResearchpeer-review

Abstract

OBJECTIVE: The purpose of this study was to determine whether human amnion epithelial cells (hAECs) can modulate the pulmonary developmental consequences of intrauterine inflammation in fetal sheep that are exposed to intraamniotic lipopolysaccharide (LPS) injection. STUDY DESIGN: At 117 days gestation, fetal sheep (n = 16) received intraamniotic LPS (20 mg). hAECs were delivered at 0, 6, and 12 hours into the fetal jugular vein (n = 4), trachea ( n = 4), or both (n = 4). Controls (n = 6) received equivalent administration of saline solution. Lungs were collected at 124 days. RESULTS: Intraamniotic LPS caused pulmonary inflammation and altered lung structure and function. hAECs attenuated changes in lung function and structure that had been induced by LPS: lung volume, 40 cm H(2)O (P <.05, intravenous + intratracheal hAECs vs LPS), tissue-to-airspace ratio (P <.05, intravenous + intratracheal hAECs vs LPS), and septal crest density (P <.001, all hAEC groups vs LPS). Leukocyte infiltration of the lungs was not reduced by hAECs; however, inflammatory cytokines were reduced (tumor necrosis factor-alpha, P <.01, vs LPS; interleukin-1b, P <.01, vs LPS; interleukin-6, P <.01 vs LPS). Surfactant protein A and C messenger RNA was increased by LPS, although this was not statistically significant (P > .05 vs control); there were significant increases in all hAEC-treated animals (surfactant protein-A, P <.05 vs LPS; surfactant protein-C, P <.01 vs LPS). CONCLUSION: Human amnion epithelial cells attenuate the fetal pulmonary inflammatory response to experimental intrauterine inflammation and reduce, but (as administered in our study) do not prevent, consequent alterations in lung development.
Original languageEnglish
Pages (from-to)e26 - e33
Number of pages8
JournalAmerican Journal of Obstetrics and Gynecology
Volume205
Issue number2 (Art. No: 156)
DOIs
Publication statusPublished - 2011

Cite this

@article{0c2fdc88dc6b4fe8b4838717b72938ce,
title = "Human amnion epithelial cells as a treatment for inflammation-induced fetal lung injury in sheep",
abstract = "OBJECTIVE: The purpose of this study was to determine whether human amnion epithelial cells (hAECs) can modulate the pulmonary developmental consequences of intrauterine inflammation in fetal sheep that are exposed to intraamniotic lipopolysaccharide (LPS) injection. STUDY DESIGN: At 117 days gestation, fetal sheep (n = 16) received intraamniotic LPS (20 mg). hAECs were delivered at 0, 6, and 12 hours into the fetal jugular vein (n = 4), trachea ( n = 4), or both (n = 4). Controls (n = 6) received equivalent administration of saline solution. Lungs were collected at 124 days. RESULTS: Intraamniotic LPS caused pulmonary inflammation and altered lung structure and function. hAECs attenuated changes in lung function and structure that had been induced by LPS: lung volume, 40 cm H(2)O (P <.05, intravenous + intratracheal hAECs vs LPS), tissue-to-airspace ratio (P <.05, intravenous + intratracheal hAECs vs LPS), and septal crest density (P <.001, all hAEC groups vs LPS). Leukocyte infiltration of the lungs was not reduced by hAECs; however, inflammatory cytokines were reduced (tumor necrosis factor-alpha, P <.01, vs LPS; interleukin-1b, P <.01, vs LPS; interleukin-6, P <.01 vs LPS). Surfactant protein A and C messenger RNA was increased by LPS, although this was not statistically significant (P > .05 vs control); there were significant increases in all hAEC-treated animals (surfactant protein-A, P <.05 vs LPS; surfactant protein-C, P <.01 vs LPS). CONCLUSION: Human amnion epithelial cells attenuate the fetal pulmonary inflammatory response to experimental intrauterine inflammation and reduce, but (as administered in our study) do not prevent, consequent alterations in lung development.",
author = "Patricia Vosdoganes and Ryan Hodges and Rebecca Lim and Alana Westover and Rutu Acharya and Euan Wallace and Timothy Moss",
year = "2011",
doi = "10.1016/j.ajog.2011.03.054",
language = "English",
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pages = "e26 -- e33",
journal = "American Journal of Obstetrics and Gynecology",
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Human amnion epithelial cells as a treatment for inflammation-induced fetal lung injury in sheep. / Vosdoganes, Patricia; Hodges, Ryan; Lim, Rebecca; Westover, Alana; Acharya, Rutu; Wallace, Euan; Moss, Timothy.

In: American Journal of Obstetrics and Gynecology, Vol. 205, No. 2 (Art. No: 156), 2011, p. e26 - e33.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Human amnion epithelial cells as a treatment for inflammation-induced fetal lung injury in sheep

AU - Vosdoganes, Patricia

AU - Hodges, Ryan

AU - Lim, Rebecca

AU - Westover, Alana

AU - Acharya, Rutu

AU - Wallace, Euan

AU - Moss, Timothy

PY - 2011

Y1 - 2011

N2 - OBJECTIVE: The purpose of this study was to determine whether human amnion epithelial cells (hAECs) can modulate the pulmonary developmental consequences of intrauterine inflammation in fetal sheep that are exposed to intraamniotic lipopolysaccharide (LPS) injection. STUDY DESIGN: At 117 days gestation, fetal sheep (n = 16) received intraamniotic LPS (20 mg). hAECs were delivered at 0, 6, and 12 hours into the fetal jugular vein (n = 4), trachea ( n = 4), or both (n = 4). Controls (n = 6) received equivalent administration of saline solution. Lungs were collected at 124 days. RESULTS: Intraamniotic LPS caused pulmonary inflammation and altered lung structure and function. hAECs attenuated changes in lung function and structure that had been induced by LPS: lung volume, 40 cm H(2)O (P <.05, intravenous + intratracheal hAECs vs LPS), tissue-to-airspace ratio (P <.05, intravenous + intratracheal hAECs vs LPS), and septal crest density (P <.001, all hAEC groups vs LPS). Leukocyte infiltration of the lungs was not reduced by hAECs; however, inflammatory cytokines were reduced (tumor necrosis factor-alpha, P <.01, vs LPS; interleukin-1b, P <.01, vs LPS; interleukin-6, P <.01 vs LPS). Surfactant protein A and C messenger RNA was increased by LPS, although this was not statistically significant (P > .05 vs control); there were significant increases in all hAEC-treated animals (surfactant protein-A, P <.05 vs LPS; surfactant protein-C, P <.01 vs LPS). CONCLUSION: Human amnion epithelial cells attenuate the fetal pulmonary inflammatory response to experimental intrauterine inflammation and reduce, but (as administered in our study) do not prevent, consequent alterations in lung development.

AB - OBJECTIVE: The purpose of this study was to determine whether human amnion epithelial cells (hAECs) can modulate the pulmonary developmental consequences of intrauterine inflammation in fetal sheep that are exposed to intraamniotic lipopolysaccharide (LPS) injection. STUDY DESIGN: At 117 days gestation, fetal sheep (n = 16) received intraamniotic LPS (20 mg). hAECs were delivered at 0, 6, and 12 hours into the fetal jugular vein (n = 4), trachea ( n = 4), or both (n = 4). Controls (n = 6) received equivalent administration of saline solution. Lungs were collected at 124 days. RESULTS: Intraamniotic LPS caused pulmonary inflammation and altered lung structure and function. hAECs attenuated changes in lung function and structure that had been induced by LPS: lung volume, 40 cm H(2)O (P <.05, intravenous + intratracheal hAECs vs LPS), tissue-to-airspace ratio (P <.05, intravenous + intratracheal hAECs vs LPS), and septal crest density (P <.001, all hAEC groups vs LPS). Leukocyte infiltration of the lungs was not reduced by hAECs; however, inflammatory cytokines were reduced (tumor necrosis factor-alpha, P <.01, vs LPS; interleukin-1b, P <.01, vs LPS; interleukin-6, P <.01 vs LPS). Surfactant protein A and C messenger RNA was increased by LPS, although this was not statistically significant (P > .05 vs control); there were significant increases in all hAEC-treated animals (surfactant protein-A, P <.05 vs LPS; surfactant protein-C, P <.01 vs LPS). CONCLUSION: Human amnion epithelial cells attenuate the fetal pulmonary inflammatory response to experimental intrauterine inflammation and reduce, but (as administered in our study) do not prevent, consequent alterations in lung development.

UR - http://www.ncbi.nlm.nih.gov/pubmed/21640967

U2 - 10.1016/j.ajog.2011.03.054

DO - 10.1016/j.ajog.2011.03.054

M3 - Article

VL - 205

SP - e26 - e33

JO - American Journal of Obstetrics and Gynecology

JF - American Journal of Obstetrics and Gynecology

SN - 0002-9378

IS - 2 (Art. No: 156)

ER -