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Maternal IL-1beta production prevents lung injury in a mouse model of bronchopulmonary dysplasia.

Artikel i vetenskaplig tidskrift
Författare Erica Bäckström
Urpo Lappalainen
Kristina Bry
Publicerad i American journal of respiratory cell and molecular biology
Volym 42
Nummer/häfte 2
Sidor 149-60
ISSN 1535-4989
Publiceringsår 2010
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Sidor 149-60
Språk en
Länkar dx.doi.org/10.1165/rcmb.2008-0287OC
Ämnesord Acute Lung Injury, genetics, pathology, physiopathology, prevention & control, Animals, Animals, Newborn, Base Sequence, Bronchopulmonary Dysplasia, genetics, pathology, physiopathology, prevention & control, DNA Primers, genetics, Disease Models, Animal, Doxycycline, pharmacology, Female, Gene Expression, drug effects, Gene Silencing, Gestational Age, Humans, Infant, Newborn, Inflammation, complications, genetics, pathology, physiopathology, Interleukin-1beta, biosynthesis, genetics, Male, Maternal-Fetal Exchange, Mice, Mice, Transgenic, Pregnancy, Pregnancy Complications, genetics, pathology, physiopathology, RNA, Messenger, genetics, metabolism, Recombinant Proteins, biosynthesis, genetics
Ämneskategorier Pediatrik

Sammanfattning

Little is known about the influence of maternal inflammation on neonatal outcome. Production of IL-1beta in the lungs of newborn infants is associated with bronchopulmonary dysplasia. Using bitransgenic (bi-TG) mice in which human (h) IL-1beta is expressed with a doxycycline-inducible system controlled by the Clara cell secretory protein promoter, we have shown that hIL-1beta expression causes a bronchopulmonary dysplasia-like illness in infant mice. To study the hypothesis that maternal hIL-1beta production modifies the response of the newborn to hIL-1beta, doxycycline was administered to bi-TG and control dams from Embryonic Day 0, inducing production of hIL-1beta by the bi-TG dams before hIL-1beta production started in their bi-TG fetuses, or from Embryonic Day 15, inducing simultaneous production of hIL-1beta by both the bi-TG dams and their bi-TG fetuses. In addition to the lungs, hIL-1beta was expressed at low levels in the uteri of bi-TG dams. Maternal inflammation preceding fetal inflammation increased the survival and growth of hIL-1beta-expressing pups, enhanced alveolarization, and protected the airways against remodeling and goblet cell hyperplasia. Maternal hIL-1beta production preceding fetal hIL-1beta production caused silencing of several inflammatory genes, including CXC and CC chemokines, murine IL-1beta, serum amyloid A3, and Toll-like receptors 2 and 4, and suppressed the expression of chitinase-like lectins Ym1 and Ym2 in the lungs of infant mice. Maternal inflammation protects the newborn against subsequent hIL-1beta-induced lung inflammation and injury. In contrast, induction of hIL-1beta production simultaneously in bi-TG dams and their fetuses offered no protection against inflammatory lung disease in the neonate.

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