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首页> 外文期刊>Infection and immunity >Respiratory-mucin inhibition of the opsonophagocytic killing of Pseudomonas aeruginosa.
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Respiratory-mucin inhibition of the opsonophagocytic killing of Pseudomonas aeruginosa.

机译：呼吸道粘蛋白抑制铜绿假单胞菌调理吞噬作用。

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Pseudomonas aeruginosa is a frequent respiratory tract colonizer in diseases in which mucociliary clearance is defective. The most striking of these is cystic fibrosis. The reasons for this organism's ability to colonize the respiratory tract and to persist there are not fully understood. Earlier studies showed that P. aeruginosa adheres preferentially to tracheobronchial mucin when compared with enterobacteria. We reasoned that if adherence to respiratory mucin protected P. aeruginosa from opsonophagocytic killing, then the ability of this organism to chronically colonize the respiratory tract could be partially explained. Using an opsonophagocytic killing assay with human polymorphonuclear leukocytes, we found that respiratory mucin protected six strains of P. aeruginosa from opsonophagocytic killing but did not protect poorly adhering strains of Escherichia coli, Staphylococcus aureus, or group B streptococci. Incubating P. aeruginosa with the mucin prior to addition to the opsonic assay inhibited phagocytic killing, whereas incubation of polymorphonuclear leukocytes with mucin did not, suggesting that inhibition was not due to an effect of mucin on leukocytes per se but was a consequence of bacterial adherence to mucin. Further studies indicated no decrease in the binding of either antibody or complement component C3 to the bacterial surface in the presence of mucin. This suggests that phagocytic inhibition may be due to a defect in uptake or destruction of mucin-coated bacteria by the leukocytes. Thus, the adherence of P. aeruginosa to respiratory mucin potentially contributes to its persistence in the respiratory tract by interfering with host immune responses.
机译：铜绿假单胞菌是粘膜纤毛清除不良的疾病中常见的呼吸道定植者。其中最引人注目的是囊性纤维化。这种生物能够在呼吸道中定植并持久存在的原因尚不完全清楚。早期的研究表明，与肠杆菌相比，铜绿假单胞菌优先粘附于气管支气管粘蛋白。我们认为，如果坚持呼吸道粘蛋白保护铜绿假单胞菌免于调理吞噬作用，则可以部分解释这种生物长期定居呼吸道的能力。使用人多形核白细胞的调理吞噬细胞杀伤试验，我们发现呼吸道粘蛋白保护了6株铜绿假单胞菌免受调理吞噬细胞的杀伤，但没有保护粘附性差的大肠杆菌，金黄色葡萄球菌或B组链球菌。将铜绿假单胞菌与粘蛋白一起孵育，然后再进行调理分析，可抑制吞噬细胞的杀伤作用，而将多形核白细胞与粘蛋白一起孵育，则表明抑制作用不是由于粘蛋白对白细胞本身的作用，而是细菌粘附的结果粘蛋白。进一步的研究表明，在粘蛋白存在下，抗体或补体成分C3与细菌表面的结合没有降低。这表明吞噬抑制作用可能是由于白细胞摄取或破坏粘蛋白包被细菌的缺陷所致。因此，铜绿假单胞菌对呼吸粘蛋白的粘附可能通过干扰宿主免疫应答而有助于其在呼吸道中的持久性。

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