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Identifying the mechanisms by which respiratory viruses predispose to secondary bacterial infections.

机译：确定呼吸道病毒易感继发细菌感染的机制。

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摘要

Antecedent viral infections predispose individuals to secondary bacterial disease, particularly in respiratory tract infections such as pneumonia, chronic obstructive pulmonary disease, otitis media and pharyngitis. Secondary bacterial infections often result in poor clinical outcomes and antibiotic treatment failure, but the mechanisms whereby viruses predispose to bacterial disease are not completely understood. We determined how infection with three ubiquitous human respiratory viruses, respiratory syncytial (RSV), human parainfluenza 3 (HPIV-3) and influenza virus alters the ability of nontypeable Haemophilus influenzae (NTHi) and Streptococcus pneumoniae to adhere to respiratory epithelial cells. RSV and HPIV-3 augmented bacterial adherence to primary bronchial epithelial cells and immortalized cell lines by up-regulating eukaryotic cell receptors for these pathogens, whereas this mechanism was less significant in primary small airway epithelial cells. Influenza virus infection enhanced bacterial adhesion but did not alter receptor expression. These studies demonstrated that the mechanisms by which viruses promote bacterial colonization vary between respiratory pathogens and are cell type-dependent.;In studies to further characterize the mechanisms by which RSV enhances bacterial adhesion, we found that RSV G glycoprotein is a receptor for NTHi and pneumococcus. NTHi and pneumococcus adhered in higher numbers to Chinese hamster ovary (CHO) cells expressing RSV G protein. Pre-incubation of CHO cells expressing RSV G protein with anti-RSV G antibodies reduced bacterial adhesion. Finally, both NTHi and pneumococci bound to RSV virions in an inoculum-dependent manner.;NTHi interacts with a number of molecules on the respiratory epithelium in order to colonize the respiratory tract. We found that NTHi uses intercellular adhesion molecule 1 (ICAM-1) expressed on respiratory epithelial cells as a receptor. NTHi adhered in higher number to CHO cells transfected with human ICAM-1 (CHQ-ICAM-1). Further studies using antibody blocking assays and western blots identified outer membrane protein PS of NTHi as a ligand for ICAM-1. Furthermore, NTHi up-regulated the expression of its own receptor, ICAM-1.;Further examination of the interactions between respiratory bacterial and viral pathogens will clarify the mechanisms responsible for secondary bacterial infections, and strategies to circumvent these processes may help reduce these complications.
机译：以前的病毒感染使个体容易患继发性细菌性疾病，尤其是在呼吸道感染中，例如肺炎，慢性阻塞性肺疾病，中耳炎和咽炎。继发性细菌感染通常会导致不良的临床结果和抗生素治疗失败，但尚不完全了解病毒易致细菌性疾病的机制。我们确定了三种普遍存在的人类呼吸道病毒，呼吸道合胞体（RSV），人类副流感3（HPIV-3）和流感病毒的感染如何改变不可分型流感嗜血杆菌（NTHi）和肺炎链球菌粘附于呼吸道上皮细胞的能力。 RSV和HPIV-3通过上调这些病原体的真核细胞受体来增强细菌对原发性支气管上皮细胞和永生化细胞系的粘附，而这种机制在原发性小气道上皮细胞中的作用较小。流感病毒感染可增强细菌粘附力，但不会改变受体表达。这些研究表明，病毒促进细菌定植的机制在呼吸道病原体之间是不同的，并且是细胞类型依赖性的。在进一步表征RSV增强细菌粘附的机制的研究中，我们发现RSV G糖蛋白是NTHi和THI的受体。肺炎球菌。 NTHi和肺炎球菌以更高数量粘附于表达RSV G蛋白的中国仓鼠卵巢（CHO）细胞。用抗RSV G抗体预孵育表达RSV G蛋白的CHO细胞可减少细菌粘附。最后，NTHi和肺炎球菌都以接种物依赖性的方式与RSV病毒体结合。NTHi与呼吸道上皮细胞上的许多分子相互作用，以使呼吸道定居。我们发现NTHi使用呼吸道上皮细胞表达的细胞间粘附分子1（ICAM-1）作为受体。 NTHi大量粘附于用人ICAM-1（CHQ-ICAM-1）转染的CHO细胞。使用抗体封闭试验和蛋白质印迹的进一步研究确定了NTHi的外膜蛋白PS作为ICAM-1的配体。此外，NTHi上调了其自身受体ICAM-1的表达；进一步检查呼吸细菌和病毒病原体之间的相互作用将阐明造成继发细菌感染的机制，而规避这些过程的策略可能有助于减少这些并发症。

著录项

  • 作者

    Avadhanula, Vasanthi.;

  • 作者单位

    The University of Tennessee Health Science Center.;

  • 授予单位 The University of Tennessee Health Science Center.;
  • 学科 Biology Virology.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 133 p.
  • 总页数 133
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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