Open AccessNeutrophil‐derived resistin release induced by Aggregatibacter actinomycetemcomitans
Author(s) -
Furugen Reiko,
Hayashida Hideaki,
Yoshii Yumiko,
Saito Toshiyuki
Publication year - 2011
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2011.02334.x
Subject(s) - resistin , aggregatibacter actinomycetemcomitans , microbiology and biotechnology , chemistry , extracellular , adipokine , neutrophil extracellular traps , biology , immunology , endocrinology , insulin resistance , inflammation , bacteria , insulin , genetics , porphyromonas gingivalis
Resistin is an adipokine that induces insulin resistance in mice. In humans, resistin is not produced in adipocytes, but in various leukocytes instead, and it acts as a proinflammatory molecule. The present investigation demonstrated high levels of resistin in culture supernatants of neutrophils that are stimulated by a highly leukotoxic strain of Aggregatibacter actinomycetemcomitans . In contrast, the level of resistin was remarkably low when neutrophils were exposed to two other strains that produce minimal levels of leukotoxin and a further isogenic mutant strain incapable of producing leukotoxin. Pretreatment of neutrophils with a monoclonal antibody to CD18, β chain of lymphocyte function‐associated molecule 1 (LFA‐1), or an Src family tyrosine kinase inhibitor before incubation with the highly leukotoxic strain inhibited the release of resistin. These results show that A. actinomycetemcomitans ‐expressed leukotoxin induces extracellular release of human neutrophil‐derived resistin by interacting with LFA‐1 on the surface of neutrophils and, consequently, activating Src family tyrosine kinases.