Bacillus cereus is recognized as a causative agent of gastrointestinal syndromes, but can also cause a devastating form of intraocular infection known as endophthalmitis. We have previously reported that the PlcR/PapR master virulence factor regulator system regulates intraocular virulence, and that the S-layer protein (SlpA) contributes to the severity of B. cereus endophthalmitis. To begin to better understand the role of other B. cereus virulence genes in endophthalmitis, expression levels of a subset of factors was measured at the midpoint of disease progression in a murine model of experimental endophthalmitis by RNA-Seq. Several cytolytic toxins were expressed at significantly higher levels in vivo than in BHI. The virulence regulators codY, gntR, and nprR were also expressed in vivo. However, at this timepoint, plcR/papR was not detectable, we previously reported that a B. cereus mutant deficient in PlcR was attenuated in the eye. The motility-related genes fla, fliF, and motB, and the chemotaxis-related gene cheA were detected during infection. We have shown previously that motility and chemotaxis phenotypes are important in B. cereus endophthalmitis. The sodA2 variant of manganese superoxide dismutase was the most highly expression gene in vivo, suggesting that this gene is criticial for intraocular survival, potentially through inhibition of neutrophil activity. Expression of the surface layer protein gene, slpA, an activator of Toll-like receptors (TLR)-2 and -4, and a potent contributor to intraocular inflammation and disease severvity, was also detected during infection, albeit at low levels. In summary, genes expressed in a mouse model of Bacillus endophthalmitis might prove to play crucial roles in the unique virulence of B. cereus endophthalmitis, and serve as candidates for novel therapies designed attenuate the severity of this often blinding infection.

中文翻译：

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眼内炎中的芽孢杆菌病毒群

蜡状芽孢杆菌被认为是胃肠道综合症的病原体，但也可以引起破坏性形式的眼内感染，称为眼内炎。我们以前曾报道过PlcR / PapR主毒力因子调节剂系统调节眼内毒力，而S层蛋白（SlpA）导致蜡状芽胞杆菌眼内炎的严重性。为了开始更好地了解其他蜡状芽孢杆菌毒力基因在眼内炎中的作用，通过RNA-Seq在实验性眼内炎的鼠模型中，在疾病进展的中点测量了一部分因子的表达水平。几种溶细胞毒素在体内的表达水平明显高于BHI。毒力调节剂codY，gntR和nprR也表达在体内。但是，在这个时间点，无法检测到plcR / papR，我们之前曾报道过缺乏PlcR的蜡状芽孢杆菌突变体在眼中减弱了。在感染过程中检测到运动相关基因fla，fliF和motB以及趋化相关基因cheA。先前我们已经证明，运动性和趋化性表型在蜡状芽孢杆菌眼内炎中很重要。锰超氧化物歧化酶的sodA2变异体是体内表达最高的基因，表明该基因可能通过抑制嗜中性粒细胞活性而批评眼内存活。表面层蛋白基因slpA（Toll样受体（TLR）-2和-4的激活物，以及眼内炎症和疾病严重程度的强力贡献者）的表达也被检测到，尽管水平很低。总之，在芽孢杆菌内眼炎小鼠模型中表达的基因可能被证明在蜡状芽胞杆菌眼内炎的独特毒力中起关键作用，并且可以作为新疗法的候选者，以减轻这种常致盲性感染的严重性。