Expression of some pathogenesis-related genes in gram-negative bacteria is controlled by bacterial cell-to-cell communication system, quorum sensing (QS), of which signal molecule is N-acylhomoserine lactone (AHL). The AHL concentration-dependent prodigiosin production in Serratia marcescens AS-1 as one of model pathogens could be suppressed by trapping AHLs onto cyclic oligosaccharide cyclodextrins (CDs). Adding CDs could suppress the prodigiosin production because the AHL concentration was kept at a low level below a threshold of the QS activation during the culture. The QS inactivation due to formation of the CD-AHL inclusion complex was demonstrated by bioassay of an AHL-synthase defective mutant, Chromobacterium violaceum CV026, in which purple pigment violacein production could be induced by adding AHLs from outside of cells. A small spot of N-hexanoyl-_L-homoserine lactone (C6HSL) solution onto an agar gel plate containing 20 wt% hydroxypropyl-β-CD and CV026 cells resulted in a meaningful reduction of violacein production after a 10-h incubation at 30℃. A quartz crystal microbalance based on admittance analysis (QCM-A) could determine stability constants between β-CD and C6HSL as (7 ± 2) × 10² M^-1.