AIM: To investigate the effect of lipopolysaccharide (LPS) on the expression and the binding characteristics of cholecystokinin receptors (CCK-R) in rat pulmonary interstitial macrophages (PIMs). METHODS: The PIMs isolated from rat lung tissues were purified by the collagenase digestion method combined with alveolar lavage and pulmonary vessel perfusion. The expression of CCK-R mRNA was detected by RT-PCR and Southe blot analysis and the binding experiments were performed by radioligand binding assay (RBA). RESULTS: CCK-A receptor (CCK-AR) and CCK-B receptor (CCK-BR) mRNA were detected in rat PIMs and their RT-PCR amplified products had a size of approximately 1.37 kb and 480 bp, respectively. The relative expression of CCK-BR mRNA was higher than that of CCK-AR mRNA after incubation with LPS for 0.5, 2, and 6 h. The expression of CCK-R mRNA could be upregulated obviously by LPS. Southe blot analysis of RT-PCR amplified CCK-AR and CCK-BR mRNA products using [γ-32p]ATP 5′-end-labelled probe showed specific hybridization bands. The specific binding of [3H] CCK-8S to rat PIM membranes was detected in the rats administered with LPS for 48 h, but not in normal rats.Scatchard analysis of the saturation curves suggested the presence of CCK-R with a high affinity (Kd=0.68+0.28 nmol/L) and a low binding capacity (Bmax=32.5+2.7 fmol.mg-1 protein) in rat PIMs. The specific binding of [3H] CCK-8S to rat PIM membranes was inhibited by unlabelled CCK-8S (ICs0=2.3±0.8 nmol/L), CCK-AR specific antagonist CR1409 (IC50=0.19±0.06 μrmol/L) and CCK-BR specific antagonist CR2945 (IC50=3.2± 1.1 nmol/L).CONCLUSION: Two types of functional CCK-AR and CCK-BR existed in rat PIMs and their expression could be upregulated by LPS.