PMID- 30244258
OWN - NLM
STAT- MEDLINE
DCOM- 20181212
LR  - 20200225
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Print)
IS  - 1234-1010 (Linking)
VI  - 24
DP  - 2018 Sep 23
TI  - Interleukin-33 (IL-33) Increases Hyperoxia-Induced Bronchopulmonary Dysplasia in 
      Newborn Mice by Regulation of Inflammatory Mediators.
PG  - 6717-6728
LID - 10.12659/MSM.910851 [doi]
AB  - BACKGROUND Interleukin-33 (IL-33) has been reported to affect chronic 
      inflammation of the lungs, but its impact on hyperoxia-injured lungs in newborns 
      remains obscure. This study aimed to investigate the role of IL-33 in the lungs 
      of neonatal mice with hyperoxia-induced bronchopulmonary dysplasia (BPD). 
      MATERIAL AND METHODS Twenty-four C57BL/6 baby mice were randomly separated into 
      three groups: the on-air group (N=16); the O2 group (N=8); and the O2 + 
      anti-IL-33 group (N=8). Forced mechanical ventilation with oxygen-rich air 
      (MV-O2) was used in 16 mouse pups. The mouse pups were incubated in containers 
      with either air or 85% O2 for 1, 3, 7, 14, 21, and 28 days after birth. At the 
      end of the treatment period, the mouse lungs were studied by histology, Western 
      blot, and quantitative real-time polymerase chain reaction (qRT-PCR) to examine 
      the expression of the pro-inflammatory mediators, including interleukin (IL)-1beta, 
      chemokine (CC motif) ligand 1 (CXCL-1), and monocyte chemoattractant protein-1 
      (MCP-1). RESULTS Following forced MV-O2, increased levels of IL-33 in whole mouse 
      lungs were associated with impaired alveolar growth and with changes consistent 
      with BPD, including reduced numbers of enlarged alveoli, increased apoptosis, and 
      increased expression of IL-1beta, CXCL-1, and MCP-1. IL-33 inhibition improved 
      alveolar development in hyperoxia-impaired lungs and suppressed IL-1beta and MCP-1 
      expression and was associated with increased transforming growth factor-beta (TGF-beta) 
      signaling, reduced pulmonary NF-kappaB activity and decreased expression of the TGF-beta 
      inhibitor SMAD-7 in forced MV-O2 exposed mouse pups. CONCLUSIONS IL-33 increased 
      hyperoxia-induced BPD in newborn mice by regulation of the expression of 
      inflammatory mediators.
FAU - Tang, Xiqin
AU  - Tang X
AD  - Department of Obstetrics and Gynecology, The First Affiliated Hospital of 
      Chongqing Medical University, Chongqing, China (mainland).
LA  - eng
PT  - Journal Article
DEP - 20180923
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL1)
RN  - 0 (Cxcl1 protein, mouse)
RN  - 0 (IL1B protein, mouse)
RN  - 0 (Il33 protein, mouse)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Interleukin-1beta)
RN  - 0 (Interleukin-33)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/metabolism
MH  - Bronchopulmonary Dysplasia/*metabolism
MH  - Chemokine CCL2
MH  - Chemokine CXCL1
MH  - Disease Models, Animal
MH  - Gene Expression Regulation/physiology
MH  - Hyperoxia/complications
MH  - Inflammation
MH  - Inflammation Mediators/*metabolism
MH  - Interleukin-1beta
MH  - Interleukin-33/*metabolism
MH  - Lung/cytology/pathology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Oxygen/metabolism
MH  - Pulmonary Alveoli/pathology
MH  - Signal Transduction
PMC - PMC6266634
COIS- Conflict of interests None.
EDAT- 2018/09/24 06:00
MHDA- 2018/12/13 06:00
PMCR- 2018/09/23
CRDT- 2018/09/24 06:00
PHST- 2018/09/24 06:00 [entrez]
PHST- 2018/09/24 06:00 [pubmed]
PHST- 2018/12/13 06:00 [medline]
PHST- 2018/09/23 00:00 [pmc-release]
AID - 910851 [pii]
AID - 10.12659/MSM.910851 [doi]
PST - epublish
SO  - Med Sci Monit. 2018 Sep 23;24:6717-6728. doi: 10.12659/MSM.910851.