Serum and glucocorticoid-inducible kinase in pulmonary tissue of preterm fetuses exposed to chorioamnionitis.
OBJECTIVE
The interaction between inflammation and transepithelial Na(+) transport is poorly understood. Chorioamnionitis has been shown to be associated with preterm labor and postnatal pulmonary morbidity of preterm infants. The human isoform of serum and glucocorticoid-inducible kinase (SGK1) is upregulated by proinflammatory cytokines and stimulates epithelial Na(+) channel ENaC and the Na(+)/K(+)-ATPase activity, an effect presumably participating in the regulation of transepithelial Na(+) transport.


METHODS
Lung tissue sections from 31 stillborn fetuses (range 21-41 weeks of gestational age) with or without chorioamnionitis were analyzed. Macrophages, neutrophils and lymphocytes were stained immunohistochemically. In addition, in situ hybridization for the detection of SGK1 mRNA was performed in fetal lung tissue. Positively labeled cells were compared by semiquantitative assessment.


RESULTS
A marked influx of macrophages into the pulmonary tissue of fetuses exposed to intrauterine inflammation when compared to fetuses without exposure to chorioamnionitis was observed (p < 0.05). There was also a tendency towards an increased density of neutrophils in fetuses exposed to chorioamnionitis. However, only small numbers of lymphocytes were detected in both groups. In fetuses exposed to chorioamnionitis, 6 of 8 fetuses did not express SGK1; however, in the group of fetuses without exposure to intrauterine inflammation 15 of 23 cases exhibited a profound SGK1 detection rate in lung tissue and airway epithelium, independent of the gestational age of the fetuses (p < 0.05).


CONCLUSIONS
Human serine threonine kinase SGK1 mRNA is observed in fetal lung tissue. On the basis of this study, we speculate that exposure to chorioamnionitis is associated with a downregulation of SGK1 in fetal lung tissue. The possible consequences of a decreased rate of SGK1 mRNA could be an impaired ability to clear the lungs from excessive fluid immediately after preterm birth.
Wirbelauer
Johannes
J
University Children's Hospital, University of Würzburg, Germany. wirbelauer_j@klinik.uni-wuerzburg.de
Schmidt
Beate
B
Klingel
Karin
K
Cao
Lei
L
Lang
Florian
F
Speer
Christian P
CP
D000028:Abortion, Induced; D000328:Adult; D002821:Chorioamnionitis / Q000097:blood / Q000201:enzymology* / Q000473:pathology; D005260:Female; D005313:Fetal Death / Q000097:blood / Q000201:enzymology* / Q000473:pathology; D015870:Gene Expression; D005865:Gestational Age; D006801:Humans; D017874:Immediate-Early Proteins / Q000235:genetics / Q000378:metabolism*; D017403:In Situ Hybridization; D008168:Lung / Q000196:embryology / Q000201:enzymology* / Q000473:pathology; D008171:Lung Diseases / Q000097:blood / Q000201:enzymology* / Q000473:pathology; D008214:Lymphocytes / Q000378:metabolism / Q000473:pathology; D008264:Macrophages / Q000378:metabolism / Q000473:pathology; D008297:Male; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D050497:Stillbirth; D000099184:Serum-Glucocorticoid Regulated Kinases
D017874:Immediate-Early Proteins; D017346:Protein Serine-Threonine Kinases; D012333:RNA, Messenger; D000099184:Serum-Glucocorticoid Regulated Kinases