Viscardi Rose M, Manimtim Winston M, Sun Chen-Chih J, Duffy Lynn, Cassell Gail H
Department of Pediatrics, University of Maryland School of Medicine, 22 S. Greene Street, Baltimore, MD 21201, USA.
Pediatr Dev Pathol. 2002 Mar-Apr;5(2):141-50. doi: 10.1007/s10024001-0134-y.
Respiratory tract colonization with Ureaplasma urealyticum in preterm infants has been associated with a higher incidence of pneumonia, severe respiratory failure, bronchopulmonary dysplasia (BPD), and death. In this report, we characterize the lung pathology and expression of tumor necrosis factor-alpha (TNF-alpha) associated with U. urealyticum pneumonia in very low-birth weight infants (VLBW; < or =1500 g). Lung pathology of archived autopsy specimens was retrospectively reviewed in three groups of VLBW infants: 5 gestational controls who died from nonpulmonary causes, 13 infants with pneumonia who were culture and/or PCR negative for U. urealyticum, and 5 infants with pulmonary disease and positive for U. urealyticum by tracheal aspirate and/or lung tissue culture or polymerase chain reaction (PCR). Presence and extent of alveolar macrophages and neutrophils, as well as interstitial lymphocytic infiltration and fibrosis were evaluated. PCR was performed on formalin-fixed, paraffin-embedded lung sections. Additional sections were immunostained for TNF-alpha. The peripheral total white blood cell counts and absolute neutrophil counts were three-fold higher in infants with U. urealyticum pneumonia than cell counts in infants infected with other organisms. There was a trend toward a predominance of neutrophils in alveoli of non- Ureaplasma pneumonia infants, but a trend toward a predominance of alveolar macrophages in U. urealyticum-infected infants. The most striking finding was the presence of increased interstitial fibrosis in all Ureaplasma-infected infants. TNF-alpha immunoreactive cell density was very low in the gestational controls, but increased in both pneumonia groups. We conclude that persistent lung U. urealyticum infection may contribute to chronic inflammation and early fibrosis in the preterm lung.
解脲脲原体在早产儿呼吸道定植与肺炎、严重呼吸衰竭、支气管肺发育不良（BPD）及死亡的较高发生率相关。在本报告中，我们描述了极低出生体重儿（VLBW；≤1500g）中与解脲脲原体肺炎相关的肺病理学特征及肿瘤坏死因子-α（TNF-α）的表达。对三组VLBW婴儿存档尸检标本的肺病理学进行了回顾性研究：5例死于非肺部原因的妊娠对照，13例肺炎婴儿，其解脲脲原体培养和/或PCR检测为阴性，以及5例肺部疾病婴儿，其气管吸出物和/或肺组织培养或聚合酶链反应（PCR）检测解脲脲原体呈阳性。评估了肺泡巨噬细胞和中性粒细胞的存在及程度，以及间质淋巴细胞浸润和纤维化情况。对福尔马林固定、石蜡包埋的肺切片进行PCR检测。额外的切片进行TNF-α免疫染色。解脲脲原体肺炎婴儿的外周全白细胞计数和绝对中性粒细胞计数比感染其他病原体的婴儿的细胞计数高三倍。非解脲脲原体肺炎婴儿的肺泡中中性粒细胞有占优势的趋势，但解脲脲原体感染婴儿的肺泡中肺泡巨噬细胞有占优势的趋势。最显著的发现是所有解脲脲原体感染婴儿均存在间质纤维化增加。TNF-α免疫反应性细胞密度在妊娠对照中非常低，但在两个肺炎组中均增加。我们得出结论，解脲脲原体在肺中的持续感染可能导致早产儿肺部的慢性炎症和早期纤维化。
