美國(guó)麻薩諸塞綜合醫(yī)院（Massachusetts General Hospital）的研究人員與Genzyme Corporation公司的研究人員合作,，研發(fā)出一種治療早產(chǎn)兒慢性肺病的方法,。這項(xiàng)研究發(fā)表在American Journal of Physiology-Lung Cellular and Molecular Physiology中,。
研究人員發(fā)現(xiàn)轉(zhuǎn)化生長(zhǎng)因子β（TGF-beta,，一種控制多種重要細(xì)胞功能的蛋白質(zhì)）的活性在一種支氣管肺發(fā)育不良（BPD）動(dòng)物模型中升高,，利用一種TGF-β抗體,，可以降低這種生長(zhǎng)因子的活性,，并改善肺臟發(fā)育,。
這項(xiàng)新研究首次證實(shí),，TGF-β是導(dǎo)致支氣管肺臟發(fā)育不良的關(guān)鍵因子，同時(shí)也會(huì)抑制受損新生兒肺臟中這種因子的活性,，因此可以降低這種疾病的嚴(yán)重性,。研究人員表示，由于支氣管肺發(fā)育不良,，是早產(chǎn)兒最重要的肺臟疾病,，因此這項(xiàng)研究的結(jié)果非常振奮人心。
之前的研究已經(jīng)證實(shí)TGF-β能幫助調(diào)節(jié)早期肺臟發(fā)育,，但是它在受到BPD破壞的成熟肺部結(jié)構(gòu)中的直接作用,，卻仍不清楚。在這項(xiàng)試驗(yàn)中,，研究人員讓一群懷孕小鼠,，于分娩前幾天注射一種TGF-β抗體或一種空白對(duì)照物質(zhì)。結(jié)果,，牠們的后代在出生后10天,，注射抗體組可以正常呼吸,，而對(duì)照組導(dǎo)致BPD。
(資料來(lái)源 : Bio.com)
原始出處：
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.
