Carlos A Rubio1. 1. Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden. carlos.rubio@ki.se
Abstract
AIMS: To audit the cellular expression of the innate antibacterial enzyme lysozyme in colonic biopsies from a cohort of patients having microscopic colitis (MC-collagenous colitis (CC) or lymphocytic colitis (LC)). Results were compared with those recorded in patients with inflammatory bowel disease (IBD) of the colon (ulcerative colitis (UC) or Crohn's colitis). METHODS: Fifty-five consecutive cases having biopsies from the left colon were investigated: 27 MC (14 CC and 13 LC) and 28 IBD (14 UC and 14 Crohn's colitis). Sections were stained with antilysozyme antibody. Twelve cases (3 CC, 3 LC, 3 UC and 3 Crohn's colitis) were challenged with the macrophage marker CD68 (clone PG-M1). RESULTS: In MC, marked lysozyme expression in the colonic crypts was recorded in CC (p<0.05). The number of cases with metaplastic Paneth cells was higher in CC than in LC (p<0.05). In IBD, only active Crohn's colitis displayed marked lysozyme expression in the colonic crypts. Marked lysozyme immune-reactivity in subepithelial lamina propria mucosa (lpm) macrophages was found in LC (LC vs CC p<0.05). CONCLUSIONS: The increased production of the antibacterial enzyme lysozyme in CC and LC supports a bacterial aetiology for these two diseases. Lysozyme upregulation in different cell types (epithelial vs macrophages) supports the notion that CC and LC might be two different maladies.
AIMS: To audit the cellular expression of the innate antibacterial enzyme lysozyme in colonic biopsies from a cohort of patients having microscopic colitis (MC-collagenous colitis (CC) or lymphocytic colitis (LC)). Results were compared with those recorded in patients with inflammatory bowel disease (IBD) of the colon (ulcerative colitis (UC) or Crohn's colitis). METHODS: Fifty-five consecutive cases having biopsies from the left colon were investigated: 27 MC (14 CC and 13 LC) and 28 IBD (14 UC and 14 Crohn's colitis). Sections were stained with antilysozyme antibody. Twelve cases (3 CC, 3 LC, 3 UC and 3 Crohn's colitis) were challenged with the macrophage marker CD68 (clone PG-M1). RESULTS: In MC, marked lysozyme expression in the colonic crypts was recorded in CC (p<0.05). The number of cases with metaplastic Paneth cells was higher in CC than in LC (p<0.05). In IBD, only active Crohn's colitis displayed marked lysozyme expression in the colonic crypts. Marked lysozyme immune-reactivity in subepithelial lamina propria mucosa (lpm) macrophages was found in LC (LC vs CC p<0.05). CONCLUSIONS: The increased production of the antibacterial enzyme lysozyme in CC and LC supports a bacterial aetiology for these two diseases. Lysozyme upregulation in different cell types (epithelial vs macrophages) supports the notion that CC and LC might be two different maladies.
Authors: Alberta Bergamo; Marco Gerdol; Alberto Pallavicini; Samuele Greco; Isabelle Schepens; Romain Hamelin; Florence Armand; Paul J Dyson; Gianni Sava Journal: Int J Mol Sci Date: 2019-11-05 Impact factor: 5.923