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beta6 Integrin subunit deficiency alleviates lung injury in a mouse model of bronchopulmonary dysplasia.

Artikel i vetenskaplig tidskrift
Författare Anna Hogmalm
Dean Sheppard
Urpo Lappalainen
Kristina Bry
Publicerad i American journal of respiratory cell and molecular biology
Volym 43
Nummer/häfte 1
Sidor 88-98
ISSN 1535-4989
Publiceringsår 2010
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Sidor 88-98
Språk en
Länkar dx.doi.org/10.1165/rcmb.2008-0480OC
Ämnesord Animals, Bronchopulmonary Dysplasia, metabolism, pathology, Chemokines, metabolism, Disease Models, Animal, Doxycycline, pharmacology, Humans, Infant, Newborn, immunology, Integrin beta Chains, metabolism, Interleukin-1beta, metabolism, Keratinocytes, cytology, Lung Diseases, metabolism, Lung Injury, metabolism, Macrophages, metabolism, Mice, Mice, Transgenic, Rats
Ämneskategorier Pediatrik

Sammanfattning

Pulmonary inflammation is associated with the development of bronchopulmonary dysplasia in premature infants. We have previously shown that perinatal pulmonary expression of human IL-1beta is sufficient to cause a lung disease similar to bronchopulmonary dysplasia, characterized by inflammation, impaired alveolarization, poor postnatal growth, and increased mortality in infant mice. The alphavbeta6 integrin plays a critical role in regulating inflammation in the adult lung. To study the role of the beta6 integrin subunit in neonatal inflammatory lung disease, we compared the pulmonary development in IL-1beta-expressing infant mice with wild-type or null beta6 integrin loci. Absence of the beta6 integrin subunit decreased the mortality and improved the postnatal growth of IL-1beta-expressing pups. The disrupted alveolar development of IL-1beta-expressing mice was improved by beta6 integrin deficiency. IL-1beta-expressing beta6(-/-) pups had shorter alveolar chord length and thinner alveolar walls than IL-1beta-expressing beta6(+/+) pups. In addition, the absence of the beta6 integrin subunit reduced IL-1beta-induced neutrophil and macrophage infiltration into the alveolar spaces. beta6 integrin subunit deficiency suppressed inflammation and goblet cell hyperplasia in the airways and alleviated airway remodeling in IL-1beta-expressing mice. The expression of the chemoattractant proteins, keratinocyte-derived chemokine, macrophage-inflammatory protein-2, calgranulin A, and calgranulin B, of osteopontin, and of the chitinase-like lectins, Ym1 and Ym2, was lower in IL-1beta-expressing beta6(-/-) than in IL-1beta-expressing beta6(+/+) mice. We conclude that absence of the beta6 integrin subunit protects the infant murine lung against IL-1beta-induced inflammation and injury.

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