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Vulnerability of the Fetal Lung to IL-1β-induced Injury is Dependent on the Time of IL-1β Production

Konferensbidrag (offentliggjort, men ej förlagsutgivet)
Författare Erica Rosenqvist
Urpo Lappalainen
Kristina Bry
Publicerad i Am J Respir Crit Care Med, Abstracts issue, april 2007. ATS conference 19-23 of may 2007.
Volym 175
Sidor A306
Publiceringsår 2007
Publicerad vid Institutionen för kliniska vetenskaper
Sidor A306
Språk en
Ämnesord inflammation, BPD, lung development
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Vulnerability of the Fetal Lung to IL-1β-induced Injury is Dependent on the Time of IL-1β Production E. Rosenqvist, U. Lappalainen, K. Bry Göteborg University, Gothenburg, Sweden Rationale: Pre- or postnatal inflammation and increased production of IL-1β are associated with the development of bronchopulmonary dysplasia in premature infants. The vulnerability of the lung to inflammatory injury during different stages of lung development is not known. We used bitransgenic CCSP-rtTA-tetO-IL-1β (bi-TG) mice in which human IL-1β is expressed in the lung epithelium with a doxycycline (dox)-inducible system, to determine the effects of IL-1β on the lung during different developmental stages. Methods: Dox was administered to pregnant dams from plug until postnatal day (PN) 7, on embryonal days (E) 15-16.5, or on E 17.5-19. Concentrations of IL-1β in lung homogenates were measured daily. Mortality, weight (Wt), and alveolar chord length of bi-TG pups and their single transgenic CCSP-rtTA (s-TG) control littermates were determined at PN 7. Results: Results on pups at PN 7 as mean±SD and time of IL-1β production are shown. Genotype Treatment Wt (g) Chord length ( m) Alive/total (%) IL-1 peak a) s-TG dox E 15-16.5 4.8 0.3 31.9 1.4 14/14 (100) none b) bi-TG dox E 15-16.5 4.8 0.5 39.4 3.1 16/16 (100) E 16-18 c) s-TG dox E 17.5-19 4.8 0.4 41.8 4.2 31/31 (100) none d) bi-TG dox E 17.5-19 4.3 0.9 70.3 14.7 12/28 (43) PN 1-3 e) s-TG dox from plug 5.0 0.4 36.2 3.1 45/47 (96) none f) bi-TG dox from plug 3.3 0.6 70.8 5.0 25/48 (52) E 16-PN 7 p≤0.05 vs. b and c; p≤0.01 vs. a and e ;p≤0.001 vs a, b, c and e Conclusions: Production of IL-1β during the saccular stage caused increased mortality, poor growth, and lack of alveolar septation in infant mice, similar to the changes caused by IL-1β production throughout the saccular and canalicular stages. Transient inflammation of the lung during the canalicular stage may disrupt alveolarization and cause BPD in premature infants.

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