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Updated: Feb 7, 2026

Subcutaneous Infection of Methicillin Resistant Staphylococcus Aureus MRSA
Published on: February 9, 2011
Role of interleukin-17 in a murine community-associated methicillin-resistant Staphylococcus aureus pneumonia model
Yasushi Shibue1, Soichiro Kimura2, Chiaki Kajiwara2
1Department of Microbiology and Infectious Diseases, Toho University School of Medicine, 5-21-16, Omori-nishi, Ota-ku, Tokyo, 143-8540, Japan; First Department of Medicine, Hokkaido University School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo, 060-8638, Japan.
Abstract:
Interleukin (IL)-17 is a key member of the Th17 cytokines and has been reported to be involved in the pathomechanisms underlying various diseases, including infectious diseases. Infections with community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) have garnered worldwide attention, and the representative USA300 strain is known to cause pneumonia in healthy people, which can be lethal. However, little is known about the role of IL-17 in CA-MRSA pneumonia. In this study, we investigated the role of IL-17 in a CA-MRSA pneumonia animal model. Mortality was higher and occurred at an earlier stage of infection in the IL-17A-knockout mice than in the wild-type (P < 0.01) and IL-17A/F-knockout mice (P < 0.05); however, no significant difference in the intrapulmonary bacterial counts was observed among the three groups of mice. Moreover, the IL-17A-knockout group showed significantly higher levels of IL-17F and granulocyte-colony stimulating factor (G-CSF) and a significantly higher neutrophil count in the bronchoalveolar lavage fluid than the other groups. These results confirmed that G-CSF expression significantly increased, and significant neutrophilic inflammation occurred under conditions of IL-17A deficiency in the murine CA-MRSA pneumonia model.
Insights
Interleukin-17A deficiency increases mortality in community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) pneumonia. IL-17A-knockout mice showed higher mortality and neutrophilic inflammation, despite similar bacterial loads.
Area of Science:
- Immunology
- Infectious Diseases
- Pulmonology
Background:
- Interleukin (IL)-17 is a critical Th17 cytokine implicated in various diseases.
- Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) causes severe pneumonia.
- The specific role of IL-17 in CA-MRSA pneumonia remains unclear.
Purpose of the Study:
- To investigate the role of IL-17 in a murine model of CA-MRSA pneumonia.
- To determine the impact of IL-17 deficiency on infection outcomes and host response.
Main Methods:
- Utilized a CA-MRSA pneumonia animal model.
- Compared outcomes in wild-type, IL-17A-knockout, and IL-17A/F-double-knockout mice.
- Assessed mortality, bacterial counts, cytokine levels (IL-17F, G-CSF), and neutrophil infiltration.
Main Results:
- IL-17A-knockout mice exhibited higher mortality at an earlier stage compared to wild-type and IL-17A/F-knockout mice.
- No significant differences in intrapulmonary bacterial counts were observed across groups.
- IL-17A deficiency led to increased IL-17F and G-CSF levels, with elevated neutrophil counts in bronchoalveolar lavage fluid.
Conclusions:
- IL-17A plays a protective role in CA-MRSA pneumonia, with its deficiency exacerbating disease severity.
- Increased G-CSF expression and neutrophilic inflammation are associated with IL-17A deficiency in this model.
- Further research into IL-17-targeted therapies for CA-MRSA infections is warranted.
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