Kwong K Y, Niang S, Literat A, Zhu N L, Ramanathan R, Jones C A, Minoo P
Division of Allergy-Immunology, Department of Pediatrics, Los Angeles County, Los Angeles, California, USA.
Life Sci. 2006 Nov 17;79(25):2349-56. doi: 10.1016/j.lfs.2006.07.040. Epub 2006 Aug 11.
Using a previously published model of human BPD this study examines whether preterm lung inflammatory cells produce transforming growth factor beta 1 (TGF-beta1), a cytokine pivotal in pathogenesis of bronchopulmonary dysplasia (BPD), and whether TGF-beta1 expression is regulated by inflammation. Lung inflammatory cells (neutrophils and macrophages) recovered in the broncho-alveolar (BAL) fluid of premature infants intubated for respiratory distress after birth expressed TGF-b1 mRNA and protein. Total and bioactive TGF-beta1 were abundantly found in the BAL fluid of the same infants. In cell culture stimulation by lipopolysaccharide (LPS) did not result in any further expression of total or bioactive TGF-beta1 by neonatal lung inflammatory cells over constitutive concentrations. In conclusion, lung inflammatory cells from premature infants are a source of TGF-beta1 but LPS does not regulate TGF-b1 production in these cells.
本研究采用先前发表的人类支气管肺发育不良（BPD）模型，探究早产肺炎症细胞是否产生转化生长因子β1（TGF-β1），这是一种在支气管肺发育不良（BPD）发病机制中起关键作用的细胞因子，以及TGF-β1的表达是否受炎症调节。出生后因呼吸窘迫而插管的早产儿支气管肺泡灌洗（BAL）液中回收的肺炎症细胞（中性粒细胞和巨噬细胞）表达TGF-β1 mRNA和蛋白。在同一婴儿的BAL液中大量发现了总TGF-β1和生物活性TGF-β1。在细胞培养中，脂多糖（LPS）刺激并未使新生儿肺炎症细胞中总TGF-β1或生物活性TGF-β1的表达超过组成型浓度。总之，早产儿的肺炎症细胞是TGF-β1的来源，但LPS并不调节这些细胞中TGF-β1的产生。
