PMID- 31268385
OWN - NLM
STAT- MEDLINE
DCOM- 20200812
LR  - 20200812
IS  - 1557-7465 (Electronic)
IS  - 1079-9907 (Print)
IS  - 1079-9907 (Linking)
VI  - 39
IP  - 11
DP  - 2019 Nov
TI  - Effect of Intranasal Instillation of Lipopolysaccharide on Lung Development and 
      Its Related Mechanism in Newborn Mice.
PG  - 684-693
LID - 10.1089/jir.2019.0006 [doi]
AB  - Premature infants are prone to repeated lung infections after birth, which can 
      disrupt the development of lung structure and function. However, the effects of 
      postnatal pulmonary inflammation on lung development in newborn mice have not 
      been reported and may play an important role in the development of 
      bronchopulmonary dysplasia (BPD). This study aimed to establish a BPD model of 
      postnatal pulmonary inflammation in premature infants and to explore its role and 
      possible mechanisms in the pathogenesis of BPD. We exposed postnatal day 1 mice 
      to lipopolysaccharide (LPS) and normal saline for 14 days. Pulmonary inflammation 
      and alveolar microvascular development were assessed by histology. In addition, 
      we also examined the expression of vascular endothelial growth factor (VEGF), 
      VEGFR2, nuclear factor-kappa-B (NF-kappaB) and related inflammatory mediators 
      [interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), macrophage 
      inflammatory protein-1alpha (MIP-1alpha), monocyte chemoattractant protein-1 (MCP-1)] in 
      the lungs. Lung histology revealed inflammatory cell infiltration, alveolar 
      simplification, and decreased microvascular density in LPS-exposed lungs. VEGF 
      and VEGFR2 expression was decreased in the lungs of LPS-exposed neonatal mice. 
      Furthermore, we detected elevated levels of the inflammatory mediators IL-1beta, 
      TNF-alpha, MIP-1alpha, and MCP-1 in the lungs, which are associated with the activation 
      of NF-kappaB. Intranasal instillation of LPS inhibits lung development in newborn 
      mice, and postnatal pulmonary inflammation may participate in the pathogenesis of 
      BPD. The mechanism is related to the inhibition of VEGF and VEGFR2 and the 
      upregulation of inflammatory mediators through activation of NF-kappaB.
FAU - You, Yaoyao
AU  - You Y
AD  - Department of Pediatrics, Yongchuan Hospital of Chongqing Medical University, 
      Chongqing, P.R. China.
FAU - Guo, Chunbao
AU  - Guo C
AD  - Department of Neonatology, Children's Hospital of Chongqing Medical University, 
      Ministry of Education Key Laboratory of Child Development and Disorders, 
      Chongqing, P.R. China.
AD  - Department of Hepatology and Liver Transplantation Center, Children's Hospital, 
      Chongqing Medical University, Chongqing, P.R. China.
FAU - Zhang, Han
AU  - Zhang H
AD  - Department of Neonatology, Children's Hospital of Chongqing Medical University, 
      Ministry of Education Key Laboratory of Child Development and Disorders, 
      Chongqing, P.R. China.
FAU - Deng, Sijun
AU  - Deng S
AD  - Department of Neonatology, Children's Hospital of Chongqing Medical University, 
      Ministry of Education Key Laboratory of Child Development and Disorders, 
      Chongqing, P.R. China.
FAU - Tang, Jia
AU  - Tang J
AD  - Department of Pediatrics, Yongchuan Hospital of Chongqing Medical University, 
      Chongqing, P.R. China.
FAU - Xu, Lingqi
AU  - Xu L
AD  - Department of Pediatrics, Yongchuan Hospital of Chongqing Medical University, 
      Chongqing, P.R. China.
FAU - Deng, Chun
AU  - Deng C
AD  - Department of Neonatology, Children's Hospital of Chongqing Medical University, 
      Ministry of Education Key Laboratory of Child Development and Disorders, 
      Chongqing, P.R. China.
FAU - Gong, Fang
AU  - Gong F
AD  - Department of Pediatrics, Yongchuan Hospital of Chongqing Medical University, 
      Chongqing, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190703
PL  - United States
TA  - J Interferon Cytokine Res
JT  - Journal of interferon & cytokine research : the official journal of the 
      International Society for Interferon and Cytokine Research
JID - 9507088
RN  - 0 (Lipopolysaccharides)
SB  - IM
MH  - Administration, Intranasal
MH  - Animals
MH  - Animals, Newborn/*metabolism
MH  - Bronchopulmonary Dysplasia/*chemically induced/pathology
MH  - Inflammation/*chemically induced/pathology
MH  - Lipopolysaccharides/*administration & dosage/*pharmacology
MH  - Lung/*drug effects/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
PMC - PMC6820870
OTO - NOTNLM
OT  - bronchopulmonary dysplasia
OT  - lipopolysaccharide
OT  - lung development
OT  - postnatal pulmonary inflammation
COIS- No competing financial interests exist.
EDAT- 2019/07/04 06:00
MHDA- 2020/08/13 06:00
PMCR- 2019/10/29
CRDT- 2019/07/04 06:00
PHST- 2019/07/04 06:00 [pubmed]
PHST- 2020/08/13 06:00 [medline]
PHST- 2019/07/04 06:00 [entrez]
PHST- 2019/10/29 00:00 [pmc-release]
AID - 10.1089/jir.2019.0006 [pii]
AID - 10.1089/jir.2019.0006 [doi]
PST - ppublish
SO  - J Interferon Cytokine Res. 2019 Nov;39(11):684-693. doi: 10.1089/jir.2019.0006. 
      Epub 2019 Jul 3.