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Maternal Pulmonary Inflammation Modulates IL-1β-induced Lung Injury in Newborn Mice

Poster (konferens)
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 A90
Publiceringsår 2007
Publicerad vid Institutionen för kliniska vetenskaper
Sidor A90
Språk en
Ämnesord BPD, inflammation, IL-1β
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Maternal Pulmonary Inflammation Modulates IL-1 -induced Lung Injury in Newborn Mice E. Rosenqvist1, U. Lappalainen1 and K. Bry1. 1Gothenburg, Gothenburg, Sweden. Rationale: Using bitransgenic CCSP-rtTA-tetO-IL-1 (bi-TG) mice in which IL-1 is expressed in the lung epithelium with a doxycycline (dox)-inducible system controlled by the CCSP promoter, we have shown that perinatal IL-1 expression causes increased mortality, poor weight gain, and poor alveolarization in the newborn mouse compared with single transgenic CCSP-rtTA (s-TG) controls (Bry AJRCMB 2006). Dox administration during pregnancy induces IL-1 production in bi-TG fetuses beginning on embryonal day (E) 14. In adult mice, IL-1 production induced by dox causes lung inflammation (Lappalainen AJRCMB 2005). It is unknown, how maternal pulmonary inflammation affects lung development in the offspring. Methods: Bi-TG and s-TG dams were mated with wild type and tetO-IL-1 males, respectively. Dox was administered either from the beginning of gestation or from E 15 until postnatal day (PN) 7. Survival, weight (Wt), alveolar chord length and, neutrophil counts in lung sections of bi-TG pups at PN 7 were assessed. Results: Results on bi-TG pups at PN 7 shown as mean SD. bi-TG dam; dox from plug (a) s-TG dam; dox from plug (b) bi-TG dam; dox from E 15 (c) s-TG dam; dox from E 15 (d) Alive/Total (%) 15/22 (68) 25/48 (52) 17/46 (37) 11/23 (48) Wt (g) 3.7 1.1 3.3 0.6 3.2 0.5 3.8 1.0 Chord length m 52.5 8.1 70.8 5.0 92.0 6.7 85.8 7.6 Neutrophils/mm2 17.1 3.9 78.4 17.0 78.5 6.0 50.4 5.6 p 0.05 vs. c; p 0.001 vs. b and c Conclusion: IL-1 production in maternal lung alleviates IL-1 -induced lung disease in newborn mice if maternal IL-1 production is initiated before fetal lung starts to produce IL-1 , but not if both maternal and fetal lung start producing IL-1 simultaneously. Thus maternal inflammation modulates fetal inflammatory responses. Maternal inflammation may protect the fetuses against inflammatory injury if maternal inflammation precedes fetal inflammation.

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