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A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Immunomodulation and Disease Tolerance to Staphylococcus aureus
Zhigang Li1, Adam G Peres2, Andreea C Damian3
1Microbiome and Disease Tolerance Center, Department of Microbiology and Immunology, McGill University, Montréal, QC, H3A 2B4, Canada. zhigang.li@mail.mcgill.ca.
Abstract:
The Gram-positive bacterium Staphylococcus aureus is one of the most frequent pathogens that causes severe morbidity and mortality throughout the world. S. aureus can infect skin and soft tissues or become invasive leading to diseases such as pneumonia, endocarditis, sepsis or toxic shock syndrome. In contrast, S. aureus is also a common commensal microbe and is often part of the human nasal microbiome without causing any apparent disease. In this review, we explore the immunomodulation and disease tolerance mechanisms that promote commensalism to S. aureus.
Insights
Staphylococcus aureus can be a dangerous pathogen or a harmless commensal. This review explores how the human immune system tolerates S. aureus, allowing it to live within the body without causing disease.
Area of Science:
- Microbiology
- Immunology
- Bacterial Pathogenesis
Background:
- Staphylococcus aureus is a leading cause of global morbidity and mortality.
- It can cause severe invasive diseases like pneumonia, sepsis, and toxic shock syndrome.
- Despite its pathogenic potential, S. aureus is also a common human commensal, particularly in the nasal microbiome.
Purpose of the Study:
- To investigate the mechanisms of immunomodulation and disease tolerance that enable Staphylococcus aureus commensalism.
- To understand how the host immune system coexists with S. aureus without initiating disease.
Main Methods:
- This is a review article, synthesizing existing research on Staphylococcus aureus-host interactions.
- Key areas explored include immune evasion strategies and host tolerance mechanisms.
- Literature search focused on studies detailing bacterial factors and host responses during commensal colonization.
Main Results:
- Commensalism is facilitated by bacterial strategies that dampen host inflammatory responses.
- Host immune tolerance mechanisms prevent excessive inflammation during S. aureus colonization.
- The balance between bacterial virulence and host immunity determines disease outcome.
Conclusions:
- Understanding S. aureus commensalism provides insights into host-pathogen dynamics.
- Mechanisms promoting disease tolerance are crucial for managing S. aureus infections.
- Further research into immunomodulation can reveal novel therapeutic targets.
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