Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Erin M Fricke; Timothy G Elgin; Huiyu Gong; Jeff Reese; Katherine N Gibson-Corley; Robert M Weiss; Kathy Zimmerman; Noelle C Bowdler; Karen M Kalantera; David A Mills; Mark A Underwood; Steven J McElroy

doi:10.1111/aji.12816

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Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Journal article

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Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood

Erin M Fricke, Timothy G Elgin, Huiyu Gong, Jeff Reese, Katherine N Gibson-Corley, Robert M Weiss, Kathy Zimmerman, Noelle C Bowdler, Karen M Kalantera, David A Mills, …

American journal of reproductive immunology (1989), Vol.79(5), pp.e12816-n/a

05/2018

DOI: 10.1111/aji.12816

PMCID: PMC5908742

PMID: 29369434

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https://www.ncbi.nlm.nih.gov/pmc/articles/5908742View

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Abstract

Premature birth complicates 10%-12% of deliveries. Infection and inflammation are the most common etiologies and are associated with increased offspring morbidity and mortality. We hypothesize that lipopolysaccharide (LPS)-induced maternal inflammation causes direct placenta injury and subsequent injury to the fetal intestine. Pregnant C57Bl6 mice were injected intraperitoneally on day 15.5 with 100 μg/kg LPS or saline. Maternal serum, amniotic fluid, placental samples, and ileal samples of offspring were obtained assessed for inflammation and/or injury. Maternal placental ultrasounds were performed. Placental DNA was isolated for microbiome analysis. Maternal injection with LPS caused elevated IL-1β, IL-10, IL-6, KC-GRO, and TNF. Placental tissue showed increased IL-1β, IL-6, and KC-GRO and decreased IL-10, but no changes were observed in amniotic fluid. Placental histology demonstrated LPS-induced increases in mineralization and necrosis, but no difference in placental blood flow. Most placentas had no detectable microbiome. Exposure to maternal LPS induced significant injury to the ilea of the offspring. Lipopolysaccharide causes a maternal inflammatory response that is mirrored in the placenta. Placental histology demonstrates structural changes; however, placental blood flow is preserved. LPS also induces an indirect intestinal injury in the offspring that lasts beyond the neonatal period.

Pregnancy

Inflammation - chemically induced

Inflammation - pathology

Pregnancy Complications - pathology

Placental Insufficiency - metabolism

Necrosis - pathology

Interleukins - metabolism

Inflammation - complications

Inflammation - metabolism

Amniotic Fluid - metabolism

Female

Digestive System Diseases - etiology

Pregnancy Complications - metabolism

Fetal Diseases - metabolism

Disease Models, Animal

Pregnancy Complications - etiology

Fetal Diseases - etiology

Placental Insufficiency - pathology

Mice, Inbred C57BL

Necrosis - metabolism

Placenta - metabolism

Placenta - blood supply

Animals

Digestive System Diseases - metabolism

Fetal Diseases - pathology

Lipopolysaccharides - pharmacology

Placenta - pathology

Mice

Regional Blood Flow - physiology

Digestive System Diseases - pathology

Placental Insufficiency - etiology

Details

Title: Subtitle: Lipopolysaccharide-induced maternal inflammation induces direct placental injury without alteration in placental blood flow and induces a secondary fetal intestinal injury that persists into adulthood
Creators: Erin M Fricke - University of Iowa, Iowa City, IA, USA
Timothy G Elgin - University of Iowa, Iowa City, IA, USA
Huiyu Gong - University of Iowa, Iowa City, IA, USA
Jeff Reese - Vanderbilt University, Nashville, TN, USA
Katherine N Gibson-Corley - University of Iowa, Iowa City, IA, USA
Robert M Weiss - University of Iowa, Iowa City, IA, USA
Kathy Zimmerman - University of Iowa, Iowa City, IA, USA
Noelle C Bowdler - University of Iowa, Iowa City, IA, USA
Karen M Kalantera - University of California, Davis, CA, USA
David A Mills - University of California, Davis, CA, USA
Mark A Underwood - University of California, Davis, CA, USA
Steven J McElroy - University of Iowa, Iowa City, IA, USA
Resource Type: Journal article
Publication Details: American journal of reproductive immunology (1989), Vol.79(5), pp.e12816-n/a
DOI: 10.1111/aji.12816
PMID: 29369434
PMCID: PMC5908742
NLM abbreviation: Am J Reprod Immunol
ISSN: 1046-7408
eISSN: 1600-0897
Publisher: Denmark
Grant note: R01 HD081121 / NICHD NIH HHS P30 DK054759 / NIDDK NIH HHS R03 DK097335 / NIDDK NIH HHS L40 DK084865 / NIDDK NIH HHS
Comment: Cover image for American Journal of Reproductive Immunology Volume 79, Issue 5
Language: English
Date published: 05/2018
Academic Unit: Microbiology and Immunology; Stead Family Department of Pediatrics; Pathology; Obstetrics and Gynecology; Internal Medicine; Ophthalmology and Visual Sciences
Record Identifier: 9983931811502771

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