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Protective effect of chorioamnionitis on the development of bronchopulmonary dysplasia triggered by postnatal systemic inflammation in neonatal rats.

Choi CW, Lee J, Oh JY, Lee SH, Lee HJ, Kim BI - Pediatr. Res. (2015)

Bottom Line: LPS significantly negated the detrimental effects of postnatal i.p.Preceding exposure to i.a.LPS protects the lungs against BPD triggered by postnatal systemic inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Seoul National University College of Medicine, Seoul, Republic of Korea.

ABSTRACT

Background: Prenatal or postnatal systemic inflammation can contribute to the development of bronchopulmonary dysplasia (BPD). We investigated whether prenatal intra-amniotic (i.a.) inflammation or early postnatal systemic inflammation can induce BPD in a rat model.

Methods: One microgram of lipopolysaccharide (LPS) or vehicle was injected into the amniotic sacs 2 d before delivery (E20). After birth, 0.25 mg/kg of LPS or vehicle was injected into the peritoneum of pups on postnatal day (P)1, P3, and P5. On P7 and P14, peripheral blood (PB), bronchoalveolar lavage fluid (BALF), and lung tissue were obtained and analyzed.

Results: Postnatal i.p. injections of LPS significantly increased neutrophil counts in PB and BALF on P7 and P14. Similarly, proinflammatory cytokine and angiogenic factor transcript levels were increased in the lung by i.p. LPS on P7. Alveolar and pulmonary vascular development was markedly disrupted by i.p. LPS on P14. However, pretreatment with i.a. LPS significantly negated the detrimental effects of postnatal i.p. LPS on PB and BALF neutrophil counts and on lung proinflammatory cytokine expression and histopathological changes.

Conclusion: Exposure to early postnatal systemic LPS induces BPD, an arrest in alveolarization, in neonatal rats. Preceding exposure to i.a. LPS protects the lungs against BPD triggered by postnatal systemic inflammation.

No MeSH data available.


Related in: MedlinePlus

Survival rates in the experimental groups. Fetal death mostly occurred in the intra-amniotic (i.a.) LPS-treated groups. After birth, most of the deaths occurred in the i.p. LPS-treated groups. Nearly half of the rats in the i.p. LPS-treated groups died during the first several days after birth. In all groups, no further mortality occurred beyond P7. Gray solid line, V+V; gray dashed line, LPS+V; black dashed line, V+LPS; black solid line, LPS+LPS. Group abbreviation: V+V, i.a. vehicle followed by i.p. vehicle-treated group; LPS+V, i.a. LPS followed by i.p. vehicle-treated group; V+LPS, i.a. vehicle followed by i.p. LPS-treated group; LPS+LPS, i.a. LPS followed by i.p. LPS-treated group. The arrowhead indicates i.a. LPS (1.0 μg/sac), and the arrows indicate postnatal i.p. LPS (0.25 mg/kg/d) administrations.
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fig2: Survival rates in the experimental groups. Fetal death mostly occurred in the intra-amniotic (i.a.) LPS-treated groups. After birth, most of the deaths occurred in the i.p. LPS-treated groups. Nearly half of the rats in the i.p. LPS-treated groups died during the first several days after birth. In all groups, no further mortality occurred beyond P7. Gray solid line, V+V; gray dashed line, LPS+V; black dashed line, V+LPS; black solid line, LPS+LPS. Group abbreviation: V+V, i.a. vehicle followed by i.p. vehicle-treated group; LPS+V, i.a. LPS followed by i.p. vehicle-treated group; V+LPS, i.a. vehicle followed by i.p. LPS-treated group; LPS+LPS, i.a. LPS followed by i.p. LPS-treated group. The arrowhead indicates i.a. LPS (1.0 μg/sac), and the arrows indicate postnatal i.p. LPS (0.25 mg/kg/d) administrations.

Mentions: The survival patterns in each group until postnatal day (P)7 are presented in Figure 2. Few fetal deaths (1/86) occurred in the i.a. vehicle-treated groups. However, the i.a. LPS-treated groups showed a modest fetal death rate of 12.2% (11/90). After birth, 51.7% (30/58) of the animals in the i.a. vehicle (V) followed by i.p. LPS-treated groups (V+LPS) and 49.0% (24/49) of the animals in the i.a. LPS followed by i.p. LPS-treated groups (LPS+LPS) died after the first i.p. LPS injection. In contrast, 88.9% (24/27) of the animals in the i.a. vehicle followed by i.p. vehicle-treated groups (V+V) and 86.7% (26/30) of the animals in the i.a. LPS followed by i.p. vehicle-treated groups (LPS+V) survived the first 7 d after birth. In all groups, no further mortality occurred beyond P7.


Protective effect of chorioamnionitis on the development of bronchopulmonary dysplasia triggered by postnatal systemic inflammation in neonatal rats.

Choi CW, Lee J, Oh JY, Lee SH, Lee HJ, Kim BI - Pediatr. Res. (2015)

Survival rates in the experimental groups. Fetal death mostly occurred in the intra-amniotic (i.a.) LPS-treated groups. After birth, most of the deaths occurred in the i.p. LPS-treated groups. Nearly half of the rats in the i.p. LPS-treated groups died during the first several days after birth. In all groups, no further mortality occurred beyond P7. Gray solid line, V+V; gray dashed line, LPS+V; black dashed line, V+LPS; black solid line, LPS+LPS. Group abbreviation: V+V, i.a. vehicle followed by i.p. vehicle-treated group; LPS+V, i.a. LPS followed by i.p. vehicle-treated group; V+LPS, i.a. vehicle followed by i.p. LPS-treated group; LPS+LPS, i.a. LPS followed by i.p. LPS-treated group. The arrowhead indicates i.a. LPS (1.0 μg/sac), and the arrows indicate postnatal i.p. LPS (0.25 mg/kg/d) administrations.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4829878&req=5

fig2: Survival rates in the experimental groups. Fetal death mostly occurred in the intra-amniotic (i.a.) LPS-treated groups. After birth, most of the deaths occurred in the i.p. LPS-treated groups. Nearly half of the rats in the i.p. LPS-treated groups died during the first several days after birth. In all groups, no further mortality occurred beyond P7. Gray solid line, V+V; gray dashed line, LPS+V; black dashed line, V+LPS; black solid line, LPS+LPS. Group abbreviation: V+V, i.a. vehicle followed by i.p. vehicle-treated group; LPS+V, i.a. LPS followed by i.p. vehicle-treated group; V+LPS, i.a. vehicle followed by i.p. LPS-treated group; LPS+LPS, i.a. LPS followed by i.p. LPS-treated group. The arrowhead indicates i.a. LPS (1.0 μg/sac), and the arrows indicate postnatal i.p. LPS (0.25 mg/kg/d) administrations.
Mentions: The survival patterns in each group until postnatal day (P)7 are presented in Figure 2. Few fetal deaths (1/86) occurred in the i.a. vehicle-treated groups. However, the i.a. LPS-treated groups showed a modest fetal death rate of 12.2% (11/90). After birth, 51.7% (30/58) of the animals in the i.a. vehicle (V) followed by i.p. LPS-treated groups (V+LPS) and 49.0% (24/49) of the animals in the i.a. LPS followed by i.p. LPS-treated groups (LPS+LPS) died after the first i.p. LPS injection. In contrast, 88.9% (24/27) of the animals in the i.a. vehicle followed by i.p. vehicle-treated groups (V+V) and 86.7% (26/30) of the animals in the i.a. LPS followed by i.p. vehicle-treated groups (LPS+V) survived the first 7 d after birth. In all groups, no further mortality occurred beyond P7.

Bottom Line: LPS significantly negated the detrimental effects of postnatal i.p.Preceding exposure to i.a.LPS protects the lungs against BPD triggered by postnatal systemic inflammation.

View Article: PubMed Central - PubMed

Affiliation: Department of Pediatrics, Seoul National University College of Medicine, Seoul, Republic of Korea.

ABSTRACT

Background: Prenatal or postnatal systemic inflammation can contribute to the development of bronchopulmonary dysplasia (BPD). We investigated whether prenatal intra-amniotic (i.a.) inflammation or early postnatal systemic inflammation can induce BPD in a rat model.

Methods: One microgram of lipopolysaccharide (LPS) or vehicle was injected into the amniotic sacs 2 d before delivery (E20). After birth, 0.25 mg/kg of LPS or vehicle was injected into the peritoneum of pups on postnatal day (P)1, P3, and P5. On P7 and P14, peripheral blood (PB), bronchoalveolar lavage fluid (BALF), and lung tissue were obtained and analyzed.

Results: Postnatal i.p. injections of LPS significantly increased neutrophil counts in PB and BALF on P7 and P14. Similarly, proinflammatory cytokine and angiogenic factor transcript levels were increased in the lung by i.p. LPS on P7. Alveolar and pulmonary vascular development was markedly disrupted by i.p. LPS on P14. However, pretreatment with i.a. LPS significantly negated the detrimental effects of postnatal i.p. LPS on PB and BALF neutrophil counts and on lung proinflammatory cytokine expression and histopathological changes.

Conclusion: Exposure to early postnatal systemic LPS induces BPD, an arrest in alveolarization, in neonatal rats. Preceding exposure to i.a. LPS protects the lungs against BPD triggered by postnatal systemic inflammation.

No MeSH data available.


Related in: MedlinePlus