Gene proteins, growth factors/their receptors in the wall of chronic calculous cholecystitis-affected gallbladder children.

Abstract

Background: Chronic calculous cholecystitis is the main cause of cholecystectomies in children, and 50.5% of patients with gallstones are asymptomatic at the time of diagnosis. However, the morphopathogenesis of chronic cholecystitis with cholelithiasis is unclear and may involve various genes, gene proteins, and growth factors.

Methods: Tissues were obtained from four males (aged 6-18 years) and two females (aged 15 and 14 years) during planned cholecystectomies. Five healthy gallbladder tissues were obtained from the archival postmortem tissue of children. SHH, IHH, HGF, IGF1, IGF1R, and HOXB3 were detected by immunohistochemistry and evaluated semiquantitatively. Statistical analysis was used to identify statistically significant differences and correlations between the factors.

Results: Decreased numbers of SHH-, IHH-, and IGF1R-positive cells, along with an increased number of HOXB3-positive cells, were observed in patients. SHH-positive epitheliocytes and connective tissue cells; IHH-positive cells in all locations; IGF1R-positive epitheliocytes, endotheliocytes, and smooth muscle cells; and HOXB3-positive smooth muscle cells were significantly different among the groups. However, the strongest negative correlation was found between HOXB3-positive smooth myocytes and SHH- and IHH-positive connective tissues, and the strongest positive correlation was detected among epithelial IHH, SHH, and IGF1R, as well as between IGF1R in the epithelium and endothelium of the blood vessels.

Conclusions: The reduced number of cells positive for the primary endodermal proteins SHH/IHH and the decreased number of IGFR1-positive cells suggest their potential roles in the development of chronic calculous cholecystitis. Additionally, the increased number of HOXB3-positive cells under these conditions likely implies stimulated growth properties, whereas HGF and IGF1 appear to have a reduced contribution to the pathogenesis of chronic calculous cholecystitis.