Lysozyme regulates LPS-induced interleukin-6 release in mice

Area of Science:

• Immunology
• Microbiology
• Biochemistry

Background:

• Bacterial lipopolysaccharide (LPS) triggers sepsis by inducing inflammatory mediators like TNF-alpha and IL-6.
• Lysozyme (LZM) has been shown to suppress LPS-induced TNF-alpha production in vivo.
• The role of LZM in modulating LPS-induced IL-6 production requires further investigation.

Purpose of the Study:

• To investigate the effect of LZM-LPS complex formation on LPS-induced IL-6 production.
• To evaluate the in vitro and in vivo efficacy of LZM-LPS complex in reducing cytokine release.

Main Methods:

• In vitro studies using mouse macrophage-like cells (RAW264.7) exposed to LPS and LZM-LPS complex.
• In vivo studies in carrageenan (CAR)-primed mice injected with LPS, LZM-LPS complex, or LZM-Escherichia coli cell complex.
• Measurement of TNF-alpha and IL-6 concentrations in cell supernatants and mouse serum.

Main Results:

• LZM-LPS complex significantly reduced both TNF-alpha and IL-6 release in vitro in a dose-dependent manner.
• In vivo, LZM-LPS complex administration markedly decreased serum IL-6 levels compared to LPS alone in CAR-primed mice.
• Even at lethal LPS doses, LZM reduced IL-6 levels, though not completely, while significantly diminishing TNF-alpha.

Conclusions:

• LZM-LPS complex formation is effective in suppressing LPS-induced IL-6 production both in vitro and in vivo.
• LZM plays a crucial role in neutralizing endotoxin and regulating systemic inflammation by inhibiting cytokine release.
• LZM demonstrates potential as a therapeutic agent for managing Gram-negative bacterial infections and sepsis.