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Interleukin-32γ transgenic mice resist LPS-mediated septic shock
Sun Jong Kim1, Siyoung Lee, Areum Kwak
1Division of Respiratory and Critical Care Medicine, Department of Internal Medicine, Kunkuk University Hospital, Konkuk University, Seoul 143-701, Republic of Korea.
Journal of Microbiology and Biotechnology
|April 19, 2014
Summary
Interleukin-32 gamma (IL-32γ) transgenic mice showed resistance to lethal endotoxemia. IL-32γ enhanced local immunity and neutrophil response while reducing systemic inflammation, suggesting a protective role in sepsis.
Area of Science:
- Immunology
- Molecular Biology
- Cytokine Research
Background:
- Interleukin-32 (IL-32) is a pro-inflammatory cytokine with multiple splicing variants.
- IL-32γ is the most active isoform, known to induce other inflammatory cytokines.
- Sepsis involves a systemic inflammatory response, often triggered by bacterial infections.
Purpose of the Study:
- To investigate the role of IL-32γ in experimental sepsis.
- To determine if IL-32γ expression influences the response to lipopolysaccharide (LPS)-induced endotoxemia.
- To elucidate the mechanisms by which IL-32γ affects local and systemic immune responses.
Main Methods:
- Generation of human IL-32γ transgenic (IL-32γ TG) mice.
- Induction of experimental sepsis using lipopolysaccharides (LPS).
- Analysis of systemic and local cytokine levels, and neutrophil influx.
Main Results:
- IL-32γ TG mice exhibited resistance to LPS-induced lethal endotoxemia.
- IL-32γ reduced systemic cytokine release post-LPS administration.
- IL-32γ promoted neutrophil influx and prolonged local cytokine production at the infection site.
Conclusions:
- IL-32γ enhances innate immune responses at the local infection site.
- IL-32γ inhibits the systemic spread of inflammatory responses during sepsis.
- IL-32γ may offer a protective effect against lethal endotoxemia by modulating immune responses.
