Anderson Mark T, Seifert H Steven
Department of Microbiology-Immunology, Northwestern University, Feinberg School of Medicine, Chicago, Illinois, United States of America.
PLoS One. 2013 Aug 16;8(8):e72183. doi: 10.1371/journal.pone.0072183. eCollection 2013.
Neisseria gonorrhoeae is the causative agent of gonorrhea and an obligate pathogen of humans. The Opa proteins of these bacteria are known to mediate attachment and internalization by host cells, including neutrophils. The Opa protein repertoire of a typical N. gonorrhoeae isolate is encoded on ~11 genes distributed throughout the chromosome and is subject to stochastic changes in expression through phase variation. Together, these characteristics make Opa proteins a critical yet unpredictable aspect of any experimental investigation into the interaction of N. gonorrhoeae with host cells. The goal of this study was to identify novel virulence factors of N. gonorrhoeae by assessing the contribution of a set of uncharacterized hydrogen peroxide-induced genes to bacterial survival against neutrophil-mediated killing. To this end, a strain harboring an engineered mutation in the NGO0322 gene was identified that exhibited increased sensitivity to neutrophil-mediated killing, enhanced internalization by neutrophils, and the ability to induce high levels of neutrophil-generated reactive oxygen species. Each of these phenotypes reverted to near wild-type levels following genetic complementation of the NGO0322 mutation. However, after immunoblot analysis of Opa proteins expressed by the isogenic parent, mutant, and genetically complemented strains, it was determined that phase variation had resulted in a disparity between the Opa profiles of these strains. To determine whether Opa phase variation, rather than NGO0322 mutation, was the cause of the observed neutrophil-related phenotypes, NGO0322 function was investigated in N. gonorrhoeae strains lacking all Opa proteins or constitutively expressing the OpaD variant. In both cases, mutation of NGO0322 did not alter survival of gonococci in the presence of neutrophils. These results demonstrate the importance of controlling for the frequent and random variation in Opa protein production by N. gonorrhoeae when investigating host cell interactions.
淋病奈瑟菌是淋病的病原体,也是人类的专性病原菌。已知这些细菌的Opa蛋白可介导包括中性粒细胞在内的宿主细胞的附着和内化。典型淋病奈瑟菌分离株的Opa蛋白库由分布在整个染色体上的约11个基因编码,并通过相变在表达上发生随机变化。这些特征共同使得Opa蛋白成为淋病奈瑟菌与宿主细胞相互作用的任何实验研究中一个关键但不可预测的方面。本研究的目的是通过评估一组未表征的过氧化氢诱导基因对细菌抵抗中性粒细胞介导杀伤的生存贡献,来鉴定淋病奈瑟菌的新型毒力因子。为此,鉴定出一株在NGO0322基因中存在工程突变的菌株,该菌株对中性粒细胞介导的杀伤表现出更高的敏感性,被中性粒细胞内化的能力增强,并且能够诱导高水平的中性粒细胞产生的活性氧。在对NGO0322突变进行基因互补后,这些表型中的每一种都恢复到接近野生型水平。然而,在对同基因亲本、突变体和基因互补菌株表达的Opa蛋白进行免疫印迹分析后,确定相变导致了这些菌株的Opa谱之间的差异。为了确定观察到的与中性粒细胞相关的表型的原因是Opa相变而非NGO0322突变,在缺乏所有Opa蛋白或组成性表达OpaD变体的淋病奈瑟菌菌株中研究了NGO0322的功能。在这两种情况下,NGO0322的突变都没有改变淋球菌在中性粒细胞存在下的存活率。这些结果表明,在研究宿主细胞相互作用时,控制淋病奈瑟菌Opa蛋白产生的频繁和随机变化非常重要。