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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

Inflammatory cytokine and angiogenic factor mRNA expression in lung tissue. The transcript levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factors (VEGF, HIF-1α) on (a) P7 (b) and P14. The transcript levels of TNF-α, IL-1β, IL-6, IL-12A, VEGF, and HIF-1α in the lung tissue were significantly higher in the V+LPS group than in the V+V group on P7. The transcript levels of TNF-α, IL-12A, VEGF remained significantly higher in the V+LPS group than in the V+V group on P14. The mRNA expression of each group is presented as the relative value to that of the V+V group. Black bars, V+V; dark gray bars, LPS+V; gray bars, V+LPS; light gray bars, 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 data are the mean ± SEM (N = 6–7 in each group). *P < 0.05 vs. V+V. HIF, hypoxia-inducible factor.
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fig6: Inflammatory cytokine and angiogenic factor mRNA expression in lung tissue. The transcript levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factors (VEGF, HIF-1α) on (a) P7 (b) and P14. The transcript levels of TNF-α, IL-1β, IL-6, IL-12A, VEGF, and HIF-1α in the lung tissue were significantly higher in the V+LPS group than in the V+V group on P7. The transcript levels of TNF-α, IL-12A, VEGF remained significantly higher in the V+LPS group than in the V+V group on P14. The mRNA expression of each group is presented as the relative value to that of the V+V group. Black bars, V+V; dark gray bars, LPS+V; gray bars, V+LPS; light gray bars, 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 data are the mean ± SEM (N = 6–7 in each group). *P < 0.05 vs. V+V. HIF, hypoxia-inducible factor.

Mentions: Proinflammatory cytokine (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factor (VEGF, hypoxia-inducible factor (HIF-1α)) transcript levels in the lung tissues were significantly higher in the V+LPS group than in the V+V group on P7 (Figure 6a). Similarly, TNF-α, IL-12A, and VEGF transcript levels on P14 were significantly higher in the V+LPS group than in the V+V group (Figure 6b). However, no differences in proinflammatory cytokine and angiogenic factor levels between the V+V and LPS+LPS groups were found on P7 and P14 (Figure 6a,b).


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)

Inflammatory cytokine and angiogenic factor mRNA expression in lung tissue. The transcript levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factors (VEGF, HIF-1α) on (a) P7 (b) and P14. The transcript levels of TNF-α, IL-1β, IL-6, IL-12A, VEGF, and HIF-1α in the lung tissue were significantly higher in the V+LPS group than in the V+V group on P7. The transcript levels of TNF-α, IL-12A, VEGF remained significantly higher in the V+LPS group than in the V+V group on P14. The mRNA expression of each group is presented as the relative value to that of the V+V group. Black bars, V+V; dark gray bars, LPS+V; gray bars, V+LPS; light gray bars, 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 data are the mean ± SEM (N = 6–7 in each group). *P < 0.05 vs. V+V. HIF, hypoxia-inducible factor.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4829878&req=5

fig6: Inflammatory cytokine and angiogenic factor mRNA expression in lung tissue. The transcript levels of proinflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factors (VEGF, HIF-1α) on (a) P7 (b) and P14. The transcript levels of TNF-α, IL-1β, IL-6, IL-12A, VEGF, and HIF-1α in the lung tissue were significantly higher in the V+LPS group than in the V+V group on P7. The transcript levels of TNF-α, IL-12A, VEGF remained significantly higher in the V+LPS group than in the V+V group on P14. The mRNA expression of each group is presented as the relative value to that of the V+V group. Black bars, V+V; dark gray bars, LPS+V; gray bars, V+LPS; light gray bars, 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 data are the mean ± SEM (N = 6–7 in each group). *P < 0.05 vs. V+V. HIF, hypoxia-inducible factor.
Mentions: Proinflammatory cytokine (TNF-α, IL-1β, IL-6, IL-12A) and angiogenic factor (VEGF, hypoxia-inducible factor (HIF-1α)) transcript levels in the lung tissues were significantly higher in the V+LPS group than in the V+V group on P7 (Figure 6a). Similarly, TNF-α, IL-12A, and VEGF transcript levels on P14 were significantly higher in the V+LPS group than in the V+V group (Figure 6b). However, no differences in proinflammatory cytokine and angiogenic factor levels between the V+V and LPS+LPS groups were found on P7 and P14 (Figure 6a,b).

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