Open AccessTHE EFFECT OF CIPROFLOXACIN ON CD14 AND TOLL-LIKE RECEPTOR-4 EXPRESSION ON HUMAN MONOCYTES
Author(s) -
Goutaro Katsuno,
Hideo Takahashi,
Hiromi Ishibashi,
Sachi Sugita,
Shuji Mori,
Shinnya Saito,
Tadashi Yoshino,
Masahiro Nishibori,
Noriaki Tanaka
Publication year - 2006
Publication title -
shock
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.095
H-Index - 117
eISSN - 1540-0514
pISSN - 1073-2322
DOI - 10.1097/01.shk.0000208803.50914.a2
Subject(s) - cd14 , tumor necrosis factor alpha , tlr4 , lipopolysaccharide , chemistry , toll like receptor , monocyte , cd16 , peripheral blood mononuclear cell , receptor , microbiology and biotechnology , immune system , innate immune system , biology , endocrinology , immunology , biochemistry , in vitro , cd8 , cd3
CD14/toll-like receptor (TLR)-4 complex on monocytes/macrophages can bind lipopolysaccharide (LPS) and transduce the signals intracellularly. An antibacterial drug, ciprofloxacin (CIP), has been reported to modulate the inflammatory and immune responses. In the present study, we examined the effects of CIP on the LPS-induced activation of monocytes isolated from human peripheral blood mononuclear cells (PBMC). CIP suppressed the expression of CD14, TLR-4, intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, and CD40 and the production of tumor necrosis factor (TNF)-alpha induced by LPS in monocytes. CIP induced the production of prostaglandin (PG)E2 and increased intracellular cyclic adenosine monophosphate (cAMP) levels. Cyclooxygenase (COX)-2 inhibitors, NS398 and indomethacin, reversed the effects of CIP on TNF-alpha production and reduced the levels of different surface antigens, whereas a protein kinase A (PKA) inhibitor, H89, did not. Therefore, CIP might regulate the TNF-alpha production induced by LPS by inhibiting the expression of LPS receptor complex, which seems to be mediated by COX-2 but not the cAMP/PKA pathway.