美国麻萨诸塞综合医院（Massachusetts General Hospital）的研究人员与Genzyme Corporation公司的研究人员合作，研发出一种治疗早产儿慢性肺病的方法。这项研究发表在American Journal of Physiology-Lung Cellular and Molecular Physiology中。
研究人员发现转化生长因子β（TGF-beta，一种控制多种重要细胞功能的蛋白质）的活性在一种支气管肺发育不良（BPD）动物模型中升高，利用一种TGF-β抗体，可以降低这种生长因子的活性，并改善肺脏发育。
这项新研究首次证实，TGF-β是导致支气管肺脏发育不良的关键因子，同时也会抑制受损新生儿肺脏中这种因子的活性，因此可以降低这种疾病的严重性。研究人员表示，由于支气管肺发育不良，是早产儿最重要的肺脏疾病，因此这项研究的结果非常振奋人心。
之前的研究已经证实TGF-β能帮助调节早期肺脏发育，但是它在受到BPD破坏的成熟肺部结构中的直接作用，却仍不清楚。在这项试验中，研究人员让一群怀孕小鼠，于分娩前几天注射一种TGF-β抗体或一种空白对照物质。结果，牠们的后代在出生后10天，注射抗体组可以正常呼吸，而对照组导致BPD。
(资料来源 : Bio.com)
原始出处：
Growth-factor Antibody May Treat Chronic Lung Disease Affecting Premature Infants
04/06/07 -- Researchers from Massachusetts General Hospital, in collaboration with scientists from the Genzyme Corporation, have identified a potential treatment for a chronic lung disease affecting premature infants. In a study to appear in the American Journal of Physiology - Lung Cellular and Molecular Physiology, which has received early online release, the scientists find that the activity of transforming growth factor-beta (TGF-beta, a protein that controls many essential cellular functions) is elevated in the lungs of an animal model of bronchopulmonary dysplasia and that treatment with an antibody to TGF-beta both decreased the growth factor's activity and improved lung development.
"Our findings show for the first time that TGF-beta is a major player in causing bronchopulmonary dysplasia and that inhibiting its activity in the injured newborn lung may decrease the severity or incidence of this disease," says Jesse Roberts Jr., MD, of the MGH departments of Anesthesia and Pediatrics and the Cardiovascular Research Center, the paper's senior author. "Since bronchopulmonary dysplasia is the most significant lung disease of premature infants, these results are very exciting."
Bronchopulmonary dysplasia (BPD) affects about 15 percent of premature infants, resulting in chronic lung disease in 10,000 to 20,000 infants in the U.S. each year, and is often caused by the mechanical ventilation and oxygen therapy required for their survival. Since BPD is more common in the most premature infants -- affecting nearly 65 percent of those with a birth weight less than 1 pound, 10 ounces -- its incidence has increased as more of the tiniest infants are surviving. The lung damage produced by BPD is usually chronic, requiring long-term treatment and frequently affecting growth and neurological development. BPD is second only to asthma as the most costly disease of children in the U.S., and infants with BPD who survive can have lung disease into adulthood.
Previous studies have shown that TGF-beta helps regulate early fetal lung development, but its direct role in the maturation of pulmonary structures disrupted by BPD has not been known. Since research at other centers has suggested that elevated TGF-beta levels might interfere with later lung development, the MGH-led team investigated that possibility and its potential relationship to BPD. A group of pregnant mice received injections of either an antibody against TGF-beta or a control substance a few days before giving birth. Their offspring were housed in either normal air or 85 percent oxygen, a concentration known to cause BPD in mice, for 10 days after birth.
