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The role of ERBB receptors in Neisseria gonorrhoeae invasion of genital epithelial cells.

机译：ERBB受体在淋病奈瑟氏球菌侵袭生殖器上皮细胞中的作用。

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摘要

Neisseria gonorrhoeae, the causative agent of the sexually transmitted infection gonorrhea, adheres to and invades genital epithelial cells. This study investigates host components that are used by the bacteria for their entry into epithelial cells. I found that the interaction of gonococci with the surface of HEC-1-B, a human endometrial carcinoma, and ME180, a human cervical epidermoid carcinoma, caused redistribution of both epidermal growth factor receptor (EGFR) and ErbB2, a related family member. Both EGFR and ErbB2 were translocated from the basolateral to the apical membrane in polarized HEC-1-B cells and concentrated under the microcolonies. Gonococcal infection increased EGFR and ErbB2 phosphorylation, indicating activation of the receptors. Kinase inhibitors of EGFR and ErbB2 inhibited and enhanced bacterial invasion, respectively, but had no effect on gonococcal adherence or the recruitment of EGFR and ErbB2 to the microcolonies. Gonococcal inoculation upregulated the transcription levels and matrix metalloproteinases (MMP)-mediated surface shedding of ligands of EGFR. Inhibition of the surface shedding of EGFR ligands by an MMP inhibitor and by heparin wash reduced gonococcal invasion without altering their adherence. N. gonorrhoeae induced the activation of the MAP Kinase ERK, PI3K/AKT and PLCgamma signaling pathways in an EGFR tyrosine kinase-dependent manner. Blocking Ca2+ flux, the downstream pathway of PLCgamma, but not ERK and PI3K by inhibitors reduced gonococcal invasion. These data indicate that N. gonorrhoeae utilizes host signaling pathways to drive its invasion. The bacteria modulates host signaling by recruiting and activating EGFR and ErbB2. N. gonorrhoeae induces EGFR activation by increasing the expression and MMP-mediated shedding of EGFR ligands.
机译：性病淋病的病原体淋病奈瑟氏球菌附着并侵袭生殖器上皮细胞。这项研究调查了细菌用于进入上皮细胞的宿主成分。我发现淋球菌与人类子宫内膜癌HEC-1-B和人类宫颈表皮样癌ME180的相互作用引起表皮生长因子受体（EGFR）和相关家族成员ErbB2的重新分布。 EGFR和ErbB2均在极化的HEC-1-B细胞中从基底外侧转移到顶膜，并在微菌落下浓缩。淋球菌感染增加了EGFR和ErbB2的磷酸化，表明受体的激活。 EGFR和ErbB2激酶抑制剂分别抑制和增强细菌侵袭，但对淋球菌粘附或EGFR和ErbB2向微菌落的募集没有影响。淋球菌接种可上调EGFR配体的转录水平和基质金属蛋白酶（MMP）介导的表面脱落。 MMP抑制剂和肝素清洗对EGFR配体表面脱落的抑制作用可减少淋球菌的侵袭，而不会改变其粘附性。淋病奈瑟氏球菌以EGFR酪氨酸激酶依赖性方式诱导MAP激酶ERK，PI3K / AKT和PLCgamma信号通路的激活。通过抑制剂阻断Ca2 +通量（PLCgamma的下游途径），但不能阻断ERK和PI3K的下游通路，从而降低了淋球菌的入侵。这些数据表明淋病奈瑟氏球菌利用宿主信号途径驱动其侵袭。该细菌通过募集和激活EGFR和ErbB2来调节宿主信号传导。淋病奈瑟氏球菌通过增加EGFR配体的表达和MMP介导的脱落来诱导EGFR激活。

著录项

  • 作者

    Swanson, Karen Victoria.;

  • 作者单位

    University of Maryland, College Park.;

  • 授予单位 University of Maryland, College Park.;
  • 学科 Biology Cell.;Biology Microbiology.
  • 学位 Ph.D.
  • 年度 2010
  • 页码 124 p.
  • 总页数 124
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

  • 入库时间 2022-08-17 11:37:13

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