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A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Staphylococcus aureus Regulator Sigma B is Important to Develop Chronic Infections in Hematogenous Murine
Lorena Tuchscherr1, Jennifer Geraci2, Bettina Löffler3
1Institute of Medical Microbiology, Jena University Hospital, Jena 07747, Germany. lorena.tuchscherrdehauschopp@med.uni-jena.de.
Abstract:
Staphylococcus aureus is a major pathogen causing bone infections that can become chronic and difficult to treat. Recently, we described the mechanism employed by S. aureus to switch to small colony variants (SCVs) and trigger intracellular bacterial persistence through the global stress regulator SigB. Here, we studied the role of SigB in the formation of chronic osteomyelitis. We used a murine hematogenous osteomyelitis model, where the mice were infected via the tail vein and subsequently developed chronic osteomyelitis. Mice were infected with S. aureus LS1, LS1ΔsigB and LS1ΔsigB complemented and kidney and bone tissues were analyzed six weeks after infection. S. aureus LS1ΔsigB formed a high rate of abscesses in kidneys, but the bacterial loads and the weight loss of the animals were lower in comparison with animals infected with the wild type and the complemented strain, indicating a more rapid and efficient bacterial clearing by the host immune system. Moreover, the sigB-mutant was not able to form SCV phenotypes either in kidney or in bone tissue. Our results demonstrate that staphylococcal SigB is important to avoid bacterial elimination by the host immune response, establish a bone infection and mediate bacterial adaptation (SCV-formation) for persistent infections.
Insights
The global stress regulator SigB in Staphylococcus aureus is crucial for establishing chronic bone infections. Its absence promotes faster bacterial clearance by the host immune system and prevents small colony variant formation.
Area of Science:
- Microbiology
- Infectious Diseases
- Immunology
Background:
- Staphylococcus aureus is a primary cause of persistent bone infections.
- Small colony variants (SCVs) are linked to intracellular bacterial persistence.
- The global stress regulator SigB mediates SCV formation in S. aureus.
Purpose of the Study:
- To investigate the role of SigB in the development of chronic osteomyelitis.
- To understand how SigB contributes to S. aureus persistence in bone infections.
Main Methods:
- A murine hematogenous osteomyelitis model was utilized.
- Mice were infected with wild-type, sigB-mutant, and complemented S. aureus strains.
- Bacterial loads, abscess formation, and SCV phenotypes in kidney and bone tissues were analyzed.
Main Results:
- Mice infected with the sigB-mutant showed reduced bacterial loads and weight loss, indicating enhanced immune clearance.
- The sigB-mutant exhibited a high rate of kidney abscesses but failed to form SCVs.
- Absence of SigB impaired the ability of S. aureus to establish persistent bone infections.
Conclusions:
- Staphylococcal SigB is essential for evading host immune responses and establishing chronic osteomyelitis.
- SigB facilitates bacterial adaptation through SCV formation, promoting persistent infections.
- Targeting SigB may offer a strategy to combat persistent S. aureus bone infections.
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