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Role of CXC Chemokine Receptor-2 in a Murine Model of Bronchopulmonary Dysplasia.

Journal article
Authors Anna Hogmalm
Erica Bäckström
Maija Bry
Urpo Lappalainen
Heikki P Lukkarinen
Kristina Bry
Published in American journal of respiratory cell and molecular biology
Volume 47
Issue 6
Pages 746-758
ISSN 1535-4989
Publication year 2012
Published at Institute of Clinical Sciences, Department of Pediatrics
Pages 746-758
Language en
Links dx.doi.org/10.1165/rcmb.2011-0394OC
Subject categories Pediatrics

Abstract

The contribution of neutrophils and CXC chemokines to the pathogenesis of bronchopulmonary dysplasia (BPD) is not well defined. Transgenic expression of interleukin (IL)-1β in the pulmonary epithelium causes lung inflammation and disrupts alveolar development in infant mice. To study the hypothesis that CXC chemokine receptor 2 (CXCR2) is a mediator of inflammatory lung injury, we compared lung development in IL-1β-expressing mice with wild-type (IL-1β/CXCR2+/+) or null (IL-1β/CXCR2-/-) CXCR2 loci. CXCR2 deficiency abolished the transmigration of neutrophils into the alveolar lumen in IL-1β-expressing mice but did not alter the number of neutrophils in the parenchyma. Deletion of CXCR2 increased the alveolar chord length and reduced the survival of the mice when IL-1β was expressed from the pseudoglandular to the alveolar stages. The capillary configuration was highly abnormal, in both IL-1β/CXCR2+/+ and IL-1β/CXCR2-/- lungs, but in very different ways. The cellular area of the parenchyma and the total capillary area of IL-1β/CXCR2+/+ and IL-1β/CXCR2-/- were smaller than those of control/CXCR2+/+ and control/CXCR2-/- mice, but the ratio of capillary area to cellular area was similar in all four genotypes. When IL-1β was expressed during the saccular stage, IL-1β/CXCR2-/- mice had smaller alveolar chord length and better survival than IL-1β/CXCR2+/+ mice. Independent of the timing of IL-1β expression, IL-1β increased alveolar septal thickness in mice with wild-type CXCR2 loci but not in CXCR2 null mice. Depending on the developmental stage at the time of the inflammatory insult, inhibition of the CXCR2-pathway may have opposite effects on alveolar septation in the neonatal lung.

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