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IL-1β expression in the distal lung epithelium disrupts lung morphogenesis and epithelial cell differentiation in fetal mice.

Artikel i vetenskaplig tidskrift
Författare Anna Hogmalm
Maija Bry
Birgitta Strandvik
Kristina Bry
Publicerad i American journal of physiology. Lung cellular and molecular physiology
Volym 306
Nummer/häfte 1
Sidor L23-L34
ISSN 1522-1504
Publiceringsår 2014
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Sidor L23-L34
Språk en
Länkar dx.doi.org/10.1152/ajplung.00154.20...
Ämnesord surfactant, inflammation, microvascular development, alveolarization, bronchopulmonary dysplasia
Ämneskategorier Pediatrik

Sammanfattning

Perinatal inflammation and the inflammatory cytokine IL-1 can modify lung morphogenesis. To examine the effects of antenatal expression of IL-1β in the distal airway epithelium on fetal lung morphogenesis, we studied lung development and surfactant expression in fetal mice expressing human IL-1β under the control of the surfactant protein (SP)-C promoter. IL-1β-expressing pups suffered respiratory failure and died shortly after birth. IL-1β caused fetal lung inflammation and enhanced the expression of keratinocyte-derived chemokine (KC/CXCL1) and monocyte chemoattractant protein 3 (MCP-3/CCL7), the calgranulins S100A8 and S100A9, the acute-phase protein serum amyloid A3 (SAA3), the chitinase-like proteins Ym1 and Ym2, and pendrin. IL-1β decreased the percentage of the total distal lung area made up of air saccules and the number of air saccules in the lungs of fetal mice. IL-1β inhibited the expression of VEGF-A and of its receptors VEGFR-1 and VEGFR-2. The percentage of the cellular area of the distal lung made up of capillaries was decreased in IL-1β-expressing fetal mice. IL-1β suppressed the production of SP-B and pro-SP-C, and decreased the amount of phosphatidylcholine and the percentage of palmitic acid in the phosphatidylcholine fraction of lung phospholipids, indicating that IL-1β prevented the differentiation of type II epithelial cells. The production of Clara cell secretory protein (CCSP) in the nonciliated bronchiolar (Clara) cells was likewise suppressed by IL-1β. In conclusion, expression of IL-1β in the epithelium of the distal airways disrupted the development of the airspaces and capillaries in the fetal lung and caused fatal respiratory failure at birth.

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http://www.gu.se/forskning/publikation/?publicationId=188184
Utskriftsdatum: 2019-09-23