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Lung pathology in premature infants with Ureaplasma urealyticum infection.

机译:解脲脲原体感染的早产儿的肺病理学。

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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.
机译:早产儿溶血性脲原体在呼吸道中的定植与肺炎,严重的呼吸衰竭,支气管肺发育不良(BPD)和死亡的发生率较高有关。在此报告中,我们表征了极低出生体重婴儿(VLBW; <或= 1500 g)与解脲支原体肺炎相关的肺部病理和肿瘤坏死因子-α(TNF-α)的表达。回顾性分析了三组VLBW婴儿的尸体解剖标本的肺部病理:5例非肺源性死亡的妊娠对照组,13例解脲支原体培养和/或PCR阴性的肺炎婴儿,以及5例肺部疾病阳性的婴儿通过气管抽吸和/或肺组织培养或聚合酶链反应(PCR)来测定解脲脲原体。评估肺泡巨噬细胞和中性粒细胞的存在和程度,以及间质性淋巴细胞浸润和纤维化。 PCR在福尔马林固定,石蜡包埋的肺切片上进行。对其他切片进行TNF-α免疫染色。解脲支原体肺炎婴儿的外周血总白细胞计数和绝对中性粒细胞计数比感染其他生物体的婴儿高三倍。非脲原体性肺炎婴儿的肺泡中嗜中性粒细胞占主导地位,而溶脲支原体感染的婴儿中肺泡巨噬细胞占主导地位。最引人注目的发现是所有感染了脲原体的婴儿间质纤维化增加。在妊娠对照组中,TNF-α免疫反应性细胞密度非常低,但在两个肺炎组中均升高。我们得出结论,持续的肺解脲支原体感染可能导致早产肺的慢性炎症和早期纤维化。

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