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Effects of murine lysozyme on lipopolysaccharide-induced biological activities

T Kurasawa1, K Takada, N Ohno

  • 1Laboratory for Immunopharmacology of Microbial Products, Tokyo University of Pharmacy and Life Science, Japan.

Insights

Murine lysozyme (M-LZM) binds to lipopolysaccharide (LPS), reducing LPS toxicity and biological activity. Both M-LZM types inhibited LPS-induced TNF-alpha production, with MP-LZM showing stronger inhibition.

Area of Science:

  • Biochemistry
  • Immunology
  • Microbiology

Background:

  • Egg-white lysozyme (EW-LZM) is known to bind lipopolysaccharide (LPS) and reduce its toxicity.
  • Lipopolysaccharide (LPS) is a major component of Gram-negative bacteria, responsible for potent inflammatory responses.
  • Lysozymes are enzymes with antibacterial properties that also interact with LPS.

Purpose of the Study:

  • To investigate the interaction between murine lysozyme (M-LZM) and lipopolysaccharide (LPS).
  • To determine if M-LZM can modulate the biological activities of LPS, similar to EW-LZM.
  • To characterize the inhibitory effects of M-LZM on LPS-induced cytokine production.

Main Methods:

  • Murine lysozyme (M-LZM) was purified from RAW264.7 cell culture supernatant using ion-exchange and gel filtration chromatography.
  • Two types of M-LZM, murine M lysozyme (MM-LZM) and murine P lysozyme (MP-LZM), were isolated.
  • Enzymatic activity assays and TNF-alpha production assays in RAW264.7 cells were performed to assess M-LZM-LPS interactions and effects.

Main Results:

  • LPS inhibited the enzymatic activities of both MM-LZM and MP-LZM, with effects influenced by temperature and ionic strength.
  • Both MM-LZM and MP-LZM inhibited LPS-induced TNF-alpha production from RAW264.7 cells.
  • MP-LZM demonstrated a stronger inhibitory effect on TNF-alpha production compared to MM-LZM.

Conclusions:

  • Murine lysozyme (M-LZM) forms complexes with LPS, similar to EW-LZM.
  • Complex formation reduces the toxicity and biological activity of LPS.
  • M-LZM plays a role in modulating inflammatory responses triggered by LPS.

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