@Article{ecn.2008.0133,
AUTHOR = {Massimiliano Mirolo, Marco Fabbri, Marina Sironi, Annunciata Vecchi, Angelo Guglielmotti, Giorgina Mangano, Giuseppe Biondi, Massimo Locati, Alberto Mantovani},
TITLE = {Impact of the anti-inflammatory agent bindarit on the chemokinome: selective inhibition of the monocyte chemotactic proteins},
JOURNAL = {European Cytokine Network},
VOLUME = {19},
YEAR = {2008},
NUMBER = {3},
PAGES = {119--122},
URL = {http://www.techscience.com/ECN/v19n3/65930},
ISSN = {1952-4005},
ABSTRACT = {Bindarit is an indazolic derivative that is devoid of any immunosuppressive effects and has no effect
on arachidonic acid metabolism. However, it has been proved to have anti-inflammatory activity in a number of
experimental diseases, including pancreatitis, arthritis, and lupus nephritis. This therapeutic effect has been
associated with its ability to interfere selectively with monocyte recruitment, although the underlying molecular
mechanisms are unknown. Here we comprehensively examine the effect of bindarit on the chemokine system, and
report that in activated monocytes and endothelial cells, it selectively inhibits the production of the monocyte
chemotactic protein subfamily of CC inflammatory chemokines (MCP-1/CCL2, MCP-3/CCL7, MCP-2/CCL8).
The capacity of bindarit to inhibit the production of a defined set of related CC chemokines by monocytes and
endothelial cells likely underlies the anti-inflammatory activity of this agent in disease. The exploitation of the
chemokine system as drug target in inflammatory disease has relied mainly on the development of receptor
antagonists and blocking antibodies. Here we report on the use of inhibition of synthesis as a potentially viable
and selective approach to modify the chemokine system.},
DOI = {10.1684/ecn.2008.0133}
}