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Human adiponectin binds to bacterial lipopolysaccharide.
Philip W Peake1, Yvonne Shen, Lesley V Campbell
1Division of Medicine, Prince of Wales Hospital, Randwick, Australia. P.Peake@unsw.edu.au
Biochemical and Biophysical Research Communications
|January 25, 2006
Summary
Adiponectin binds to lipopolysaccharide (LPS), a key inflammatory molecule. This interaction suggests adiponectin acts as an anti-inflammatory agent in conditions like atherosclerosis.
Area of Science:
- Biochemistry
- Immunology
- Endocrinology
Background:
- Adiponectin is recognized for its roles in insulin sensitivity and energy homeostasis.
- It also possesses anti-inflammatory and anti-atherogenic properties, notably suppressing lipopolysaccharide (LPS)-mediated inflammation.
Purpose of the Study:
- To investigate the direct binding interaction between adiponectin and lipopolysaccharide (LPS).
- To elucidate the conditions and molecular components influencing this interaction.
Main Methods:
- Demonstration of direct binding between recombinant/native adiponectin and LPS from three bacterial species.
- Assessment of binding kinetics under varying pH conditions and in the presence/absence of cations (Ca(2+), Mg(2+)) and chelators (EDTA).
- Evaluation of the inhibitory effects of various molecules (Lipid A, C1q, heparin, zymosan, sugars) and modifications to adiponectin (deglycosylation, reduction, alkylation).
Main Results:
- Adiponectin directly binds to LPS.
- The interaction is pH-dependent, occurring optimally at pH 6.0, and is modulated by divalent cations and EDTA.
- Binding is inhibited by periodate-mediated deglycosylation and reduction/alkylation of adiponectin, indicating the importance of its structure.
Conclusions:
- Adiponectin directly interacts with LPS, suggesting a mechanism for its anti-inflammatory effects.
- Adiponectin may function as a scavenger molecule in inflammatory sites like atherosclerosis, binding to LPS and other pro-inflammatory agents.