Laboratory of Infection and Immunity, West China Medical Center, Sichuan University, Chengdu.
Acta Biochim Biophys Sin (Shanghai). 2011 Sep;43(9):680-7. doi: 10.1093/abbs/gmr064. Epub 2011 Jul 21.
Since bacterial invasion into host cells is an important step in the infection process, using the agents to interfere with bacterial internalization is an attractive approach to block the infection process. In this work, we describe a new, previously unrecognized role of the human cationic host defense peptide HMGN2 during Klebsiella pneumoniae infections. Our results revealed that the internalization of K. pneumoniae strain 03183 into cultured bladder epithelial cells (T24) was significantly reduced at HMGN2 concentrations that were unable to produce any bacteriostatic or bactericidal effect. Using microarrays and follow-up studies, we demonstrated that HMGN2 affected the internalization of K. pneumoniae strain 03183 by inhibiting the attachment of bacteria, and then decreasing bacteria-induced ERK1/2 activation and actin polymerization, which might contribute to bacterial internalization into T24 cells. This disruption of bacterial internalization implied that HMGN2 could provide protection against K. pneumoniae infections.
由于细菌侵入宿主细胞是感染过程中的重要步骤，因此使用这些药物来干扰细菌内化是阻止感染过程的一种有吸引力的方法。在这项工作中，我们描述了人源阳离子宿主防御肽 HMGN2 在肺炎克雷伯菌感染过程中的一个新的、以前未被认识到的作用。我们的结果表明，在 HMGN2 浓度下，不能产生任何抑菌或杀菌作用的情况下，肺炎克雷伯菌菌株 03183 进入培养的膀胱上皮细胞（T24）的内化明显减少。通过使用微阵列和后续研究，我们证明 HMGN2 通过抑制细菌的附着来影响肺炎克雷伯菌菌株 03183 的内化，然后降低细菌诱导的 ERK1/2 激活和肌动蛋白聚合，这可能有助于细菌内化进入 T24 细胞。这种细菌内化的破坏意味着 HMGN2 可以为肺炎克雷伯菌感染提供保护。
