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Updated: Aug 20, 2026
Fast and Specific Assessment of the Halogenating Peroxidase Activity in Leukocyte-enriched Blood Samples
Published on: July 28, 2016
Superoxide production from human polymorphonuclear leukocytes by human mannan-binding protein (MBP)
Kazuhide Uemura1, Harumi Yamamoto, Tomoaki Nakagawa
1Department of Biological Chemistry, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501 Japan.
Abstract:
Mannan-binding protein (MBP) is a Ca(2+)-dependent mammalian lectin that plays an important role in innate immunity. In this study, we found that ligand-bound MBP stimulates polymorphonuclear leukocytes (PMN) to induce cell aggregation and superoxide production. The biological response of PMN to ligand-bound MBP was dose- and time-dependent. The PMN aggregation and superoxide production induced by ligand-bound MBP was blocked completely by pertussis toxin, and partially blocked by a platelet activation factor receptor antagonist, TCV-309. These findings suggest that the ligand-bound MBP stimulates PMN through a putative MBP receptor(s) on PMN.
Insights
Ligand-bound Mannan-binding protein (MBP) activates immune cells called polymorphonuclear leukocytes (PMN), causing aggregation and superoxide production. This suggests a specific receptor on PMN mediates MBP
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Mannan-binding protein (MBP) is a calcium-dependent lectin crucial for innate immunity.
- MBP recognizes microbial carbohydrates, initiating immune responses.
- The precise mechanisms by which MBP interacts with immune cells are under investigation.
Purpose of the Study:
- To investigate the effects of ligand-bound MBP on polymorphonuclear leukocytes (PMN).
- To elucidate the signaling pathways involved in MBP-mediated PMN activation.
- To identify potential receptors for MBP on PMN.
Main Methods:
- Incubation of PMN with ligand-bound MBP.
- Measurement of PMN aggregation.
- Assay of superoxide production by PMN.
- Inhibition studies using pertussis toxin and a platelet activation factor receptor antagonist (TCV-309).
Main Results:
- Ligand-bound MBP dose- and time-dependently stimulated PMN aggregation and superoxide production.
- Pertussis toxin completely blocked the observed PMN responses.
- A platelet activation factor receptor antagonist partially inhibited the responses.
Conclusions:
- Ligand-bound MBP activates PMN, leading to aggregation and superoxide release.
- The activation process involves G-protein signaling, as indicated by pertussis toxin sensitivity.
- These findings suggest the existence of a specific MBP receptor on PMN that mediates these cellular responses.
