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An antimicrobial peptide tachyplesin acts as a secondary secretagogue and amplifies lipopolysaccharide‐induced hemocyte exocytosis
Author(s) -
Ozaki Aya,
Ariki Shigeru,
Kawabata Shunichiro
Publication year - 2005
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2005.04800.x
Subject(s) - exocytosis , secretion , innate immune system , antimicrobial peptides , lipopolysaccharide , microbiology and biotechnology , biology , secretagogue , beta defensin , immune system , biochemistry , immunology , antimicrobial
In the horseshoe crab, bacterial lipopolysaccharide (LPS) induces exocytosis by granular hemocytes, resulting in the secretion of various defense molecules, such as lectins and antimicrobial peptides, via a G protein‐mediating signaling pathway. This response is a key component of the horseshoe crab innate immune response against infectious microorganisms. Here, we report an endogenous amplification mechanism for LPS‐induced hemocytes exocytosis. The concentration of LPS required for maximal secretion decreased in proportion to the density of hemocytes, suggesting the presence of a positive feedback mechanism for secretion via a mediator secreted from hemocytes. The exocytosed fluid of hemocytes was found able to induce hemocyte exocytosis in the absence of LPS. Furthermore, tachyplesin, a major antimicrobial peptide of hemocytes, was able to trigger exocytosis in an LPS‐independent manner, which was inhibited by a phospholipase C inhibitor, U‐73122, and a G protein inhibitor, pertussis toxin. Surface plasmon resonance analysis showed that tachyplesin directly interacts with bovine G protein. These findings suggest that the tachyplesin‐induced hemocyte exocytosis also occurs via a G protein‐mediating signaling pathway. We concluded that tachyplesin functions not only as an antimicrobial substance, but also as a secondary secretagogue of LPS‐induced hemocyte exocytosis, leading to the amplification of the innate immune reaction at sites of injury.