Journal
PEDIATRIC RESEARCH
Volume 60, Issue 2, Pages 141-146Publisher
NATURE PUBLISHING GROUP
DOI: 10.1203/01.pdr.0000228322.73777.05
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Funding
- NCRR NIH HHS [P512RR13986] Funding Source: Medline
- NHLBI NIH HHS [HL04492, HL52636, HL71113, HL075432] Funding Source: Medline
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Chronic inflammation and fibrosis are hallmarks of lung pathology of newborn Ureaplasma infection. We hypothesized that antenatally acquired Ureaplasma stimulates a chronic inflammatory, profibrotic immune response that contributes to lung injury, altered developmental signaling, and fibrosis. Lung specimens from 125-d gestation baboon newborns ventilated for 14 d that were either infected antenatally with Ureaplasma serovar I or noninfected, and 125-d and 140-d gestational controls were obtained from the Baboon BPD Resource Center (San Antonio, TX). Trichrome stain to assess fibrosis and immunohistochemistry for alpha-smooth muscle actin (alpha-SMA) and transforming growth factor beta(1) (TGF beta(1)) were performed. Lung homogenates were analyzed by enzyme-linked immunosorbent assay (ELISA) for cytokines [tumor necrosis factor alpha (TNF alpha), interleukin (IL)-1 beta, TGF beta(1), oncostatin M (OSM), IL-10, and interferon gamma (IFN gamma)] and the chemokine MCP-1 and by Western blot for Smad2, Smad3, and Smad7. Compared with noninfected ventilated and gestational controls, Ureaplasma-infected lungs demonstrated more extensive fibrosis, increased alpha-SMA and TGF beta, immunostaining, and higher concentrations of active TGF beta(1), IL-1 beta, and OSM, but no difference in IL-10 levels. There was a trend toward higher Smad2/Smad7 and Smad3/Smad7 ratios in Ureaplasma lung homogenates, consistent with up-regulation of TGF beta(1) signaling. Collectively, these data suggest that a prolonged proinflammatory response initiated by intrauterine Ureaplasma infection contributes to early fibrosis and altered developmental signaling in the immature lung.
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