Kruger T, Baier J
Department of Pediatrics, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
Infect Immun. 1997 Dec;65(12):5131-6. doi: 10.1128/iai.65.12.5131-5136.1997.
Bronchopulmonary dysplasia (BPD) is a chronic lung disease of premature infants who are mechanically ventilated due to respiratory distress. The disease consists of an initial inflammatory influx of neutrophils to the lungs, followed by long-term chronic fibrosis of the lung tissue. The antigenic repertoire that initiates the inflammatory component of BPD has not been defined. Furthermore, the repertoire of cytokines responsible for attracting neutrophils to the lung and the mediators of pathogenesis in BPD have not been characterized. Mycoplasmas such as Mycoplasma hominis and Ureaplasma urealyticum have been isolated from the lungs of infants that developed BPD and yet have not been widely recognized as potential initiators of the inflammatory component of BPD. In the studies described here, we examined the ability of both viable and heat-killed Mycoplasma hominis to elicit type II epithelial cell production of cytokines that are chemotactic for polymorphonuclear leukocytes (PMNs), particularly interleukin-8 (IL-8) and epithelial cell-derived neutrophil-activating peptide (ENA-78). The results of these studies demonstrate that M. hominis and M. hominis antigen are potent stimulators of type II epithelial cell-derived IL-8 and ENA-78. Thus, these data strongly suggest that the presence of M. hominis in the lungs of premature infants may initiate the inflammatory component of BPD by inducing epithelial cell production of cytokines chemotactic for PMNs. Furthermore, these data suggest that the onset of the inflammatory component of BPD likely precedes, and is independent of, the recruitment and activation of alveolar macrophages.
支气管肺发育不良(BPD)是一种因呼吸窘迫而接受机械通气的早产儿慢性肺部疾病。该疾病最初表现为中性粒细胞向肺部的炎症性浸润,随后是肺组织的长期慢性纤维化。引发BPD炎症成分的抗原库尚未明确。此外,负责将中性粒细胞吸引至肺部的细胞因子库以及BPD发病机制的介质也未得到表征。人型支原体和解脲脲原体等支原体已从患BPD的婴儿肺部分离出来,但尚未被广泛认可为BPD炎症成分的潜在引发因素。在本文所述的研究中,我们检测了活的和热灭活的人型支原体诱导II型上皮细胞产生对多形核白细胞(PMN)具有趋化作用的细胞因子的能力,特别是白细胞介素-8(IL-8)和上皮细胞衍生的中性粒细胞激活肽(ENA-78)。这些研究结果表明,人型支原体和人型支原体抗原是II型上皮细胞衍生的IL-8和ENA-78的强效刺激物。因此,这些数据强烈表明,早产儿肺部存在人型支原体可能通过诱导上皮细胞产生对PMN具有趋化作用的细胞因子来引发BPD的炎症成分。此外,这些数据表明,BPD炎症成分的发作可能先于肺泡巨噬细胞的募集和激活,且与之无关。