Published online Dec 21, 2021. doi: 10.3748/wjg.v27.i47.8138
Peer-review started: March 12, 2021
First decision: May 1, 2021
Revised: May 12, 2021
Accepted: December 7, 2021
Article in press: December 7, 2021
Published online: December 21, 2021
Processing time: 279 Days and 13.4 Hours
Chromofungin (CHR: chromogranin-A 47-66) is a chromogranin-A derived peptide with anti-inflammatory and anti-microbial properties. Ulcerative colitis (UC) is characterized by a colonic decrease of CHR and a dysregulation of dendritic CD11c+ cells.
To investigate the association between CHR treatment and dendritic cells (DCs)-related markers in different immune compartments in colitis.
A model of acute UC-like colitis using dextran sulphate sodium (DSS) was used in addition to biopsies collected from UC patients.
Intrarectal CHR treatment reduced the severity of DSS-induced colitis and was associated with a significant decrease in the expression of CD11c, CD40, CD80, CD86 and interleukin (IL)-12p40 in the inflamed colonic mucosa and CD11c, CD80, CD86 IL-6 and IL-12p40 within the mesenteric lymph nodes and the spleen. Furthermore, CHR treatment decreased CD80 and CD86 expression markers of splenic CD11c+ cells and decreased NF-κB expression in the colon and of splenic CD11c+ cells. In vitro, CHR decreased CD40, CD80, CD86 IL-6 and IL-12p40 expression in naïve bone marrow-derived CD11c+ DCs stimulated with lipopolysaccharide. Pharmacological studies demonstrated an impact of CHR on the NF-κB pathway. In patients with active UC, CHR level was reduced and showed a negative linear relationship with CD11c and CD86.
CHR has protective properties against intestinal inflammation via the regulation of DC-related markers and CD11c+ cells. CHR could be a potential therapy of UC.
Core Tip: Ulcerative colitis (UC) is characterized by a colonic decrease of chromofungin (CHR: chromogranin-A 47-66) and a dysregulation of CD11c+ dendritic cells (DC). Using a UC-like model (dextran sulphate sodium) and biopsies collected from UC patients, we demonstrated a protective effect of CHR via the regulation of DC-related markers and CD11c+ cells at the colonic, mesenteric lymph node and spleen levels, through a potential effect via the NF-κB pathway. In patients with active UC, CHR level showed a negative linear relationship with CD11c+ marker. CHR could be a potential therapy of UC, but larger samples and additional experiments are needed.