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Updated: Oct 10, 2026
A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection
O Takeuchi1, K Hoshino, S Akira
1Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan. Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Osaka, Japan.
Abstract:
Toll-like receptor (TLR) family acts as pattern recognition receptors for pathogen-specific molecular patterns. We previously showed that TLR2 recognizes Gram-positive bacterial components whereas TLR4 recognizes LPS, a component of Gram-negative bacteria. MyD88 is shown to be an adaptor molecule essential for TLR family signaling. To investigate the role of TLR family in host defense against Gram-positive bacteria, we infected TLR2- and MyD88-deficient mice with Staphylococcus aureus. Both TLR2- and MyD88-deficient mice were highly susceptible to S. aureus infection, with more enhanced susceptibility in MyD88-deficient mice. Peritoneal macrophages from MyD88-deficient mice did not produce any detectable levels of cytokines in response to S. aureus. In contrast, TLR2-deficient macrophages produced reduced, but significant, levels of the cytokines, and TLR4-deficient macrophages produced the same amounts as wild-type cells, indicating that S. aureus is recognized not only by TLR2, but also by other TLR family members except for TLR4.
Insights
Toll-like receptor 2 (TLR2) and MyD88 are crucial for host defense against Staphylococcus aureus. MyD88-deficient mice showed greater susceptibility, indicating MyD88
Area of Science:
- Immunology
- Microbiology
Background:
- Toll-like receptors (TLRs) are key pattern recognition receptors.
- TLR2 recognizes Gram-positive bacterial components, while TLR4 recognizes Gram-negative bacterial LPS.
- MyD88 is an essential adaptor molecule for TLR signaling.
Purpose of the Study:
- To investigate the role of TLRs and MyD88 in host defense against Staphylococcus aureus.
- To determine which TLRs are involved in recognizing S. aureus.
Main Methods:
- Infection of TLR2- and MyD88-deficient mice with S. aureus.
- Analysis of susceptibility and cytokine production in macrophages.
Main Results:
- Both TLR2- and MyD88-deficient mice exhibited high susceptibility to S. aureus.
- MyD88-deficient mice showed more severe susceptibility than TLR2-deficient mice.
- MyD88-deficient macrophages failed to produce cytokines in response to S. aureus.
- TLR2-deficient macrophages produced reduced cytokine levels, while TLR4-deficient macrophages produced normal levels.
Conclusions:
- TLR2 and MyD88 are critical for host defense against S. aureus.
- S. aureus is recognized by TLR2 and other TLR family members, but not TLR4.
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