The Toxicity Mechanisms of <i>Staphylococcus aureus</i> Exposure in <i>Caenorhabditis elegans</i>

Huang Hongfei; Cai Yiwei; Li Guiying; Wong Po Keung; An Taicheng

doi:10.12052/gdutxb.250086

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The Toxicity Mechanisms of Staphylococcus aureus Exposure in Caenorhabditis elegans

更新时间：2026-08-04

- The Toxicity Mechanisms of Staphylococcus aureus Exposure in Caenorhabditis elegans
- Vol. 43, Issue 4, Pages: 39-46(2026)
- 作者机构：
  
  1. 广东工业大学环境健康与污染控制研究院,广东,广州,510006
  2. 广东工业大学环境科学与工程学院,广东,广州,510006
  3. 粤港澳污染物暴露与健康联合实验室,广东,广州,510006
  4. 环境催化与健康风险控制重点实验室,广东,广州,510006
- 作者简介：
- 基金信息：
- DOI：10.12052/gdutxb.250086
  CLC： X17/R994
- Published：2026
- 稿件说明：
移动端阅览
黄鸿飞, 蔡仪威, 李桂英, 等. 金黄色葡萄球菌暴露对秀丽隐杆线虫的毒性机制研究[J]. 广东工业大学学报, 2026, 43(4): 39-46.
黄鸿飞, 蔡仪威, 李桂英, 等. 金黄色葡萄球菌暴露对秀丽隐杆线虫的毒性机制研究[J]. 广东工业大学学报, 2026, 43(4): 39-46. DOI： 10.12052/gdutxb.250086.

DOI： 10.12052/gdutxb.250086

摘要

致病菌引发的感染性疾病已成为全球公共卫生安全的重大威胁。现有研究主要集中于阐明典型野生型(Wild Type

WT)致病菌的急性毒力机制，但对活的不可培养(Viable But Non-culturable

VBNC) 状态致病菌的宿主感染方式、毒性大小及其致病机理等方面的研究仍比较缺乏。因此，本文以秀丽隐杆线虫(

Caenorhabditis elegans

C. elegans

) 为模式宿主，构建了金黄色葡萄球菌(包括VBNC状态)(

Staphylococcus aureus

S. aureus

)−秀丽隐杆线虫感染体系。感染后，通过裂解技术将暴露后的线虫体内的金黄色葡萄球菌释放出来。进一步观察线虫体内金黄色葡萄球菌的状态变化、毒力蛋白释放以及毒力基因表达等情况，并揭示金黄色葡萄球菌在不同状态下进入线虫后的感染机理。结果表明：野生型金黄色葡萄球菌在线虫体内会加速繁殖并定植于其肠道。同时野生型致病菌可释放大量毒力蛋白，引发线虫急性感染；而VBNC状态的金黄色葡萄球菌的繁殖能力、定植能力均较弱。值得注意的是，VBNC状态金黄色葡萄球菌能够在线虫体内适宜环境下发生复苏，复苏率高达到90.4%，是体外自然复苏效率的6倍。此外，野生型金黄色葡萄球菌通过大规模上调其毒力基因表达来突破宿主免疫防御；而VBNC状态金黄色葡萄球菌则表现出不同的致病模式。首先其毒力基因表达延迟，会优先激活生物膜形成相关基因以创造复苏条件，随后通过应激响应系统逐步恢复毒力基因表达，最终重建致病能力并引发线虫慢性感染。这种独特的毒力复苏机制使VBNC状态金黄色葡萄球菌能够在宿主免疫压力下实现长期定植。因此，很有必要对环境系统中典型致病菌及其VBNC状态的致病菌的毒性进行长期监测来避免潜在的健康风险。

Abstract

Infectious diseases caused by pathogenic bacteria pose a critical threat to global public health security. However

existing research predominantly focuses on elucidating the acute virulence mechanisms of typical cultura

ble (Wild-Type

WT) pathogenic bacteria

whereas studies on the host infection modes

virulence levels

and pathogenic mechanisms of viable but non-culturable (VBNC) state pathogens are notably lacking. Therefore

this study established a

Staphylococcus aureus

(

S. aureus

) (including VBNC state) -

Caenorhabditis elegans

(

C. elegans

) infection system. Following infection

S. aureus

within exposed nematodes was released via lysis techniques to investigate bacterial state transitions

virulence protein secretion

and virulence gene expression patterns

aiming to elucidate infection mechanisms under distinct bacterial states. Findings of this research revealed that wild-type

S. aureus

exhibited accelerated proliferation and intestinal colonization in nematodes

accompanied by substantial virulence protein release

triggering acute infection. In contrast

VBNC-state

S. aureus

displayed significantly reduced reproductive and colonization capacities. Notably

VBNC-state

S. aureus

underwent resuscitation within the nematode host

achieving a resuscitation rate of 90.4%

representing a sixfold increase compared with natural resuscitation

in vitro

. Furthermore

wild-type

S. aureus

subverted host immune defenses through global upregulation of virulence gene expression. Conversely

VBNC-state

S. aureus

exhibited a distinct pathogenic pattern: delayed virulence gene expression

prioritized activation of biofilm formation-related genes to establish resuscitation conditions

followed by gradual restoration of virulence gene expression through stress response systems

ultimately re-establishing pathogenicity and inducing chronic infection. This unique virulence resuscitation mechanism facilitates VBNC-state

S. aureus

in maintaining long-term colonization under host immune pressure. Consequently

long-term monitoring of both typica

l pathogenic bacteria and their VBNC-state counterparts in environmental systems is imperative to prevent potential health risks.

关键词

Keywords

references

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The Toxicity Mechanisms of Staphylococcus aureus Exposure in Caenorhabditis elegans

DOI：10.12052/gdutxb.250086

摘要

Abstract

关键词

Keywords

references