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Surfactant protein-A enhances ureaplasmacidal activity in vitro
Adora C Okogbule-Wonodi1, Kirsty L Chesko, Mobolaji E Famuyide
1Department of Pediatrics, School of Medicine, University of Maryland-Baltimore (UMB), 29 S. Greene St., Baltimore, MD 21201, USA.
Insights
Surfactant protein-A (SP-A) enhances the clearance and killing of Ureaplasma bacteria by immune cells in vitro. This suggests SP-A plays a key role in protecting preterm infants from Ureaplasma infections.
Area of Science:
- Pulmonary immunology
- Neonatal infectious diseases
- Host-pathogen interactions
Background:
- Persistent Ureaplasma spp. colonization in preterm infants is a risk factor for bronchopulmonary dysplasia (BPD).
- Surfactant protein-A (SP-A), crucial for bacterial clearance and inflammation control, is deficient in preterm lungs.
- SP-A deficient mice show impaired Ureaplasma clearance and heightened inflammation.
Purpose of the Study:
- To investigate the role of SP-A in Ureaplasma clearance in vitro.
- To analyze SP-A binding to Ureaplasma isolates.
- To assess SP-A-mediated phagocytosis and killing of Ureaplasma by macrophages.
Main Methods:
- Analysis of SP-A binding to Ureaplasma isolates.
- Assessment of SP-A-mediated phagocytosis of Ureaplasma by RAW 264.7 macrophages.
- Measurement of Ureaplasma killing activity by macrophages pre-incubated with SP-A.
Main Results:
- SP-A binding to Ureaplasma was calcium-dependent and similar across isolates.
- SP-A enhanced Ureaplasma phagocytosis by macrophages.
- SP-A increased macrophage killing of Ureaplasma by 2.1-fold.
- SP-A reduced Ureaplasma-stimulated TNF-α release but not TGF-β1 release.
Conclusions:
- SP-A enhances Ureaplasma clearance and reduces inflammation in vitro.
- These findings highlight SP-A's importance in host defense against perinatal Ureaplasma infections.
- SP-A may be a therapeutic target for preventing BPD in preterm infants.
Background:
Persistent respiratory tract colonization with Ureaplasma spp. in preterm infants is a significant risk factor for the development of the chronic lung disorder, bronchopulmonary dysplasia (BPD). Surfactant protein-A (SP-A), a lung collectin critical for bacterial clearance and regulating inflammation, is deficient in the preterm lung. In an experimental Ureaplasma-pneumonia model, infected SP-A deficient mice exhibited delayed bacterial clearance and an exaggerated inflammatory response compared to infected wild-type mice. The objective was to analyze the role of SP-A in Ureaplasma clearance in vitro.
Subjects And Methods:
We analyzed SP-A binding to Ureaplasma isolates and SP-A-mediated ureaplasmal phagocytosis and killing by cultured RAW 264.7 macrophages.
Results:
Calcium-dependent SP-A binding was similar among Ureaplasma isolates tested. Pre-incubation of RAW 264.7 cells with SP-A (10-50 μg/ml) enhanced phagocytosis of fluorescein-isothiocyanate (FITC)-labeled Ureaplasma. Surfactant protein-A also increased ureaplasmacidal activity of RAW 264.7 cells by 2.1-fold over 4 h. Pre-incubation of RAW 264.7 cells with 10 μg/ml SP-A reduced lipopolysaccharide (LPS) (100 ng/ml) and Ureaplasma (10(6) color changing units/ml)-stimulated release of tumor necrosis factor-α (TNF-α) by 46% and 43%, respectively, but did not affect transforming growth factor β(1) (TGFβ(1)) release.
Conclusions:
These in vitro data confirm that SP-A is important in host defense to perinatally-acquired Ureaplasma infection.
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