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首页> 外文期刊>Infection and immunity >Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells
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Klebsiella pneumoniae Capsule Polysaccharide Impedes the Expression of β-Defensins by Airway Epithelial Cells

机译：肺炎克雷伯氏菌胶囊多糖阻碍气道上皮细胞表达β-防御素

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Human β-defensins (hBDs) contribute to the protection of the respiratory tract against pathogens. It is reasonable to postulate that pathogens have developed countermeasures to resist them. Klebsiella pneumoniae capsule polysaccharide (CPS), but not the lipopolysaccharide O antigen, mediated resistance against hBD1 and hBD2. hBD3 was the most potent hBD against Klebsiella. We investigated the possibility that as a strategy for survival in the lung, K. pneumoniae may not activate the expression of hBDs. Infection of A549 and normal human bronchial cells with 52145-ΔwcaK2, a CPS mutant, increased the expression of hBD2 and hBD3. Neither the wild type nor the lipopolysaccharide O antigen mutant increased the expression of hBDs. In vivo, 52145-ΔwcaK2 induced higher levels of mBD4 and mBD14, possible mouse orthologues of hBD2 and hBD3, respectively, than the wild type. 52145-ΔwcaK2-dependent upregulation of hBD2 occurred via NF-κB and mitogen-activated protein kinases (MAPKs) p44/42, Jun N-terminal protein kinase (JNK)-dependent pathways. The increase in hBD3 expression was dependent on the MAPK JNK. 52145-ΔwcaK2 engaged Toll-like receptors 2 and 4 (TLR2 and TLR4) to activate hBD2, whereas hBD3 expression was dependent on NOD1. K. pneumoniae induced the expression of CYLD and MKP-1, which act as negative regulators for 52145-ΔwcaK2-induced expression of hBDs. Bacterial engagement of pattern recognition receptors induced CYLD and MKP-1, which may initiate the attenuation of proinflammatory pathways. The results of this study indicate that K. pneumoniae CPS not only protects the pathogen from the bactericidal action of defensins but also impedes their expression. These features of K. pneumoniae CPS may facilitate pathogen survival in the hostile environment of the lung.
机译：人β-防御素（hBD）有助于保护呼吸道免受病原体侵害。可以合理地假设病原体已经开发出抵抗它们的对策。肺炎克雷伯氏菌荚膜多糖（CPS）而非脂多糖O抗原介导了对hBD1和hBD2的抗性。 hBD3是针对 Klebsiella 的最有效的hBD。我们调查了 K作为肺部生存策略的可能性。肺炎可能不会激活hBDs的表达。用CPS突变体52145-Δ wca K2 感染A549和正常人支气管细胞，可增加hBD2和hBD3的表达。野生型和脂多糖O抗原突变体均不增加hBD的表达。 体内，52145-Δ wca K2 诱导的mBD4和mBD14的水平高于野生动物，可能是hBD2和hBD3的小鼠直系同源物类型。 52145-Δ wca K2 依赖的hBD2上调是通过NF-κB和有丝分裂原激活的蛋白激酶（MAPK）p44 / 42，Jun N端蛋白激酶（JNK）引起的）依赖的途径。 hBD3表达的增加取决于MAPK JNK。 52145-Δ wca K2 参与Toll样受体2和4（TLR2和TLR4）激活hBD2，而hBD3的表达依赖于NOD1。 K。肺炎诱导CYLD和MKP-1的表达，它们是52145-Δ wca K2 诱导的hBDs表达的负调控因子。模式识别受体的细菌参与诱导了CYLD和MKP-1，这可能启动促炎途径的减弱。这项研究的结果表明 K。肺炎 CPS不仅可以保护病原体免受防御素的杀菌作用，还可以阻止其表达。 K的这些功能。肺炎CPS可能有助于病原体在肺部不利环境中存活。

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