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A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Maternal lipopolysaccharide-induced inflammation during pregnancy programs impaired offspring innate immune responses
Ron Beloosesky1, Nir Maravi, Zeev Weiner
1Department of Obstetrics/Gynecology, Rambam Medical Center, Haifa, Israel. tomor2304@yahoo.com
Insights
Maternal exposure to lipopolysaccharides during pregnancy suppresses the offspring's innate immune response. This suggests prenatal inflammation may increase a newborn's susceptibility to infections.
Area of Science:
- Immunology
- Developmental Biology
- Perinatal Medicine
Background:
- The fetal immune system matures during gestation, with early inflammatory pathway activation potentially impacting immune competency.
- Understanding the long-term effects of prenatal inflammatory exposures is crucial for neonatal health.
Purpose of the Study:
- To investigate the impact of maternal lipopolysaccharide exposure on the developing fetal immune system.
- To determine if prenatal inflammation affects the innate immune response of offspring to inflammatory stimuli.
Main Methods:
- Pregnant rats received lipopolysaccharides or saline solution at 18 days gestation.
- Offspring were assessed at postnatal day 24 for plasma cytokine levels following lipopolysaccharide challenge.
- Key cytokines measured included interleukin-6, interleukin-1beta, tumor necrosis factor-alpha, and interleukin-10.
Main Results:
- Offspring of dams exposed to lipopolysaccharides showed significantly reduced levels of interleukin-6, interleukin-1beta, tumor necrosis factor-alpha, and interleukin-10.
- This indicates a suppressed innate immune response in pups exposed to prenatal inflammation.
Conclusions:
- Maternal lipopolysaccharide exposure during pregnancy suppresses the innate immune response of offspring.
- Prenatal inflammatory exposures may impair neonatal immune defenses, increasing vulnerability to infections.
Objective:
Because the fetal innate immune system is responsive, while still maturing during the preterm period, we hypothesized that the early activation of fetal inflammatory pathways may have an impact on the ultimate expression of immune competency.
Study Design:
Pregnant Sprague Dawley rats (n = 7; Harlan Sprague Dawley Inc, Jerusalem, Israel) at 18 days gestation received intraperitoneal injections of saline solution or lipopolysaccharides (500 microg/kg). Pups were delivered spontaneously. At postnatal day 24, pups received intraperitoneal lipopolysaccharide (100 microg/kg), and plasma cytokine levels were measured before and 4 hours after lipopolysaccharide administration.
Results:
In response to lipopolysaccharides, pups of the lipopolysaccharide-injected dams had significantly (P < .05) reduced interleukin-6 (median [25th,75th percentile], 229 [84,6086] vs 4745 [2765,6643] pg/mL), interleukin-1beta (median [25th,75th percentile], 820 [125,1196] vs 1682 [1515,2127] pg/mL), tumor necrosis factor-alpha (median [25th,75th percentile], 4.8 [1.2,91] vs 163 [46,205] pg/mL), and interleukin-10 responses, when compared with saline solution-injected dams.
Conclusion:
Maternal lipopolysaccharide exposure suppresses offspring innate immune response to inflammatory stimuli. These results suggest that maternal inflammatory exposures during pregnancy may impair newborn infant innate responses and increase susceptibility to infection.
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