Cholecystokinin octapeptide inhibits the in vitro expression of CD14 in rat pulmonary interstitial macrophages induced by lipopolysaccharide.
- Author:
Shujin LI
1
;
Bin CONG
;
Yunli YAN
;
Yuxia YAO
;
Chunling MA
;
Yiling LING
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cells, Cultured; Culture Media, Conditioned; chemistry; Female; Lipopolysaccharide Receptors; biosynthesis; Lipopolysaccharides; pharmacology; Macrophages, Alveolar; cytology; drug effects; metabolism; Rats; Rats, Sprague-Dawley; Sincalide; pharmacology; Specific Pathogen-Free Organisms; Tumor Necrosis Factor-alpha; drug effects; secretion
- From: Chinese Medical Journal 2002;115(2):276-279
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo study the effect of cholecystokinin octapeptide (CCK-8) on lipopolysaccharide (LPS)-stimulated pulmonary interstitial macrophages (PIM) in vitro.
METHODSPIM were isolated and cultured in the presence or absence of LPS, CCK-8, proglumide (the antagonist of CCK receptors) and vehicle. The expression of membrane CD14 (mCD14) protein was assayed by flow cytometry and soluble CD14 (sCD14) in the supernatant was analyzed semi-quantitatively by Western blot. TNF-alpha in the supernatant was detected with ELISA.
RESULTSCCK-8, at concentrations of 10(-7) mol/L and 10(-6) mol/L, significantly inhibited the expression of mCD14. Release of sCD14 and TNF-alpha in the supernatant was up-regulated by LPS (1 microg/ml) but reduced by CCK-8. The effect of CCK-8 was inhibited by proglumide.
CONCLUSIONCCK-8 negatively modulated several functions of LPS-stimulated PIM through CCK receptors. This may be one of the mechanisms for CCK-8 to alleviate inflammation in lung tissue during endotoxemia.
