在新生儿和人上皮细胞模型中,细小脲原体和解脲原体诱导不同类型的炎症。

IF 3.1 3区 医学 Q1 PEDIATRICS
Hongzhen Zhu, Pol Oliveras-Julià, Gea F Hasperhoven, Luca L van Leeuwen, Ad C J M de Bruijn, Marijn C Verwijs, Annemarie M C van Rossum, René F Kornelisse, Kim Stol, Wendy W J Unger
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引用次数: 0

摘要

背景:早产儿支气管肺发育不良(BPD)的发生与感染和炎症有关。细小脲原体和解脲原体都与BPD有关。方法:对25例早产儿气管吸入物的细菌存在和炎症介质进行分析。用细小乌球菌和解脲乌球菌感染肺泡上皮细胞,评估炎症介质、细胞死亡和氧化应激。结果:2/25的新生儿检出细小乌菌,3/25的新生儿检出解脲乌菌。3/5尿原体阳性标本共检出大肠杆菌。细小乌菌阳性样品中IL-6、IL-8和CXCL5含量较高。铀脲阳性样品中IL-6和IL-8含量高,CXCL5含量低,CXCL1和CCL2含量高。与解脲脲相比,细小乌菌感染的细胞培养物中检测到的IL-6水平高出5至10倍,IL-8水平高出2倍,而在解脲脲感染的培养物中检测到细胞凋亡。两种细菌感染均可诱导ROS。结论:正如在BPD中观察到的那样,两种脲原体都可能通过氧化应激导致炎症和细胞损伤,但机制不同。细小球菌感染诱导肺泡上皮细胞强烈的促炎介质反应,而解脲球菌感染导致细胞死亡。影响:解脲球菌和细小球菌可通过分泌炎症介质导致慢性肺部疾病中的炎症和细胞损伤。这两种菌的作用机制不同:细小球菌感染可诱导肺泡上皮细胞强烈的促炎介质反应,而解脲球菌感染可导致上皮细胞死亡。我们的数据为尿原体在早产儿慢性肺病发展中的作用提供了新的见解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ureaplasma parvum and Ureaplasma urealyticum induce distinct types of inflammation in neonates and human epithelial cell models.

Background: Development of bronchopulmonary dysplasia (BPD) in premature neonates is associated with infection and inflammation. Both Ureaplasma parvum and Ureaplasma urealyticum are associated with BPD. We examined whether there is a difference in pathogenicity between the two species METHODS: Tracheal aspirates of 25 preterm neonates were analyzed for bacterial presence and inflammatory mediators. Alveolar epithelial cells were infected with U. parvum and U. urealyticum strains to assess inflammatory mediators, cell death and oxidative stress.

Results: U. parvum was detected in 2/25 and U. urealyticum in another 3/25 neonates. E. coli was co-detected in 3/5 Ureaplasma-positive samples. U. parvum-positive samples contained high IL-6, IL-8 and CXCL5. U. urealyticum-positive samples also contained high IL-6 and IL-8, but low CXCL5, and high CXCL1 and CCL2. Five-to-ten-fold higher IL-6 and two-fold higher IL-8 levels were detected in U. parvum-infected cell cultures than U. urealyticum, whereas apoptotic cell death was detected in U. urealyticum-infected cultures. Infection with both species induced ROS.

Conclusion: Both Ureaplasma species may contribute to inflammation and cell damage, via oxidative stress, as observed in BPD, yet through different mechanisms. U. parvum infection induces a strong pro-inflammatory mediator response in alveolar epithelial cells while U. urealyticum infection results in cell death.

Impact: U. urealyticum and U. parvum can contribute to the inflammation and cell damage seen in chronic lung disease through the secretion of inflammatory mediators. The two species differ in their mechanism of action: U. parvum infection induces a strong pro-inflammatory mediator response in alveolar epithelial cells while U. urealyticum infection results in epithelial cell death. Our data provide new insights into the role of Ureaplasma in the development of chronic lung disease in premature infants.

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来源期刊
Pediatric Research
Pediatric Research 医学-小儿科
CiteScore
6.80
自引率
5.60%
发文量
473
审稿时长
3-8 weeks
期刊介绍: Pediatric Research publishes original papers, invited reviews, and commentaries on the etiologies of children''s diseases and disorders of development, extending from molecular biology to epidemiology. Use of model organisms and in vitro techniques relevant to developmental biology and medicine are acceptable, as are translational human studies
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