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Updated: Jun 11, 2025
Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
Intraspecific cooperation allows the survival of Staphylococcus aureus staff: a novel strategy for disease relapse
Hua Luo1,2, Lijia Ni1,2, Tongling Chen1,2
1Department of Clinical Laboratory, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, 510120, China.
Background:
The contribution of interspecies interactions between coinfecting pathogens to chronic refractory infection by affecting pathogenicity is well established. However, little is known about the impact of intraspecific interactions on infection relapse, despite the cross-talk of different strains within one species is more common in clinical infection. We reported a case of chronic refractory pulmonary infection relapse, caused by two methicillin-sensitive S. aureus (MSSA) strains (SA01 and SA02) and revealed a novel strategy for relapse via intraspecific cooperation.
Methods:
The hemolytic ability, growth curve, biofilm formation, virulence genes and response of G. mellonella larvae to S. aureus infection were analysed to confirm this hypothesis.
Results:
SA02 hemolytic activity was inhibited by SA01, along with the expression of hemolysin genes and the virulence factor Hla. Additionally, SA01 significantly enhanced the biofilm formation of SA02. AIP-RNAIII may be a possible pathway for this interaction. Compared with mono-infection, a worse outcome (decreased larval survival and increased microbial burden) of the two MSSA strains coinfected with G. mellonella confirmed that intraspecific interactions indeed enhanced bacterial survival in vivo.
Conclusion:
The intraspecific interaction of S. aureus could lead to chronic refractory infection via pathogenicity changes.
Insights
Intraspecific cooperation between two methicillin-sensitive Staphylococcus aureus (MSSA) strains led to chronic refractory pulmonary infection. This bacterial interaction enhanced pathogenicity and promoted infection relapse, highlighting a novel mechanism in persistent infections.
Area of Science:
- Microbiology
- Infectious Diseases
- Bacterial Pathogenesis
Background:
- Interspecies pathogen interactions are known to affect pathogenicity in chronic infections.
- The role of intraspecific interactions between different strains of the same pathogen in infection relapse remains largely unexplored.
- Clinical infections frequently involve cross-talk between multiple strains of a single species.
Purpose of the Study:
- To investigate the impact of intraspecific interactions between two Staphylococcus aureus strains on chronic refractory infection.
- To elucidate the mechanisms by which intraspecific cooperation influences pathogenicity and infection relapse.
- To report a novel strategy for infection relapse mediated by intraspecific cooperation.
Main Methods:
- Analysis of hemolytic activity, growth curves, and biofilm formation of S. aureus strains.
- Assessment of virulence gene expression, including hemolysin genes and Hla.
- Evaluation of G. mellonella larval response to mono- and coinfection with S. aureus strains.
- Investigation of the potential role of AIP-RNAIII in mediating intraspecific interactions.
Main Results:
- One S. aureus strain (SA01) inhibited the hemolytic activity and hemolysin gene expression of another strain (SA02).
- SA01 significantly enhanced biofilm formation in SA02, suggesting a cooperative strategy.
- Coinfection with both MSSA strains resulted in worse outcomes in G. mellonella larvae, including decreased survival and increased microbial burden, compared to mono-infection.
- AIP-RNAIII was identified as a potential mediator of this intraspecific interaction.
Conclusions:
- Intraspecific interactions among Staphylococcus aureus strains can alter pathogenicity.
- Bacterial cooperation between strains can lead to enhanced virulence and contribute to chronic, refractory infections.
- Understanding intraspecific interactions is crucial for developing effective strategies against persistent bacterial infections.
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