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
Ulcerative colitis (UC) is a disorder in which the gastrointestinal tract becomes ulcerated and inflamed. Although treatments and therapeutic strategies are evolving quickly, treatments are still inadequate for a substantial percentage of those with active UC, and some therapies may have serious adverse side effects. Therefore, UC needs new therapeutic approaches associated with higher efficacy and limited side effects. In UC, there is an overactivation of innate immune cells such as macrophages and dendritic cells (DCs). Recently, in the context of UC and experimental colitis, new data highlighted an essential anti-inflammatory role of chromofungin (CHR), a chromogranin-A derived peptide, on peritoneal macrophages.
To evaluate CHR's effects on different DCs at various immune compartments and to define a potential intracellular pathway implicated.
To investigate the association between CHR treatment and DCs-related markers in colitis.
Participants with active UC and a model of acute UC-like colitis using dextran sulphate sodium were used. We used cell culture and quantitative reverse transcription-polymerase chain reaction to analyze the relative expression levels of CD11c, CD80, CD86, interleukin (IL)-6 and IL-12p40 within the colonic samples, mesenteric lymph nodes and the spleen.
In a preclinical setting, CHR treatment the expression of CD11c, CD40, CD80, CD86 and IL-12p40 in the inflamed colonic mucosa and CD11c, CD80, CD86, IL-6 and IL-12p40 within the mesenteric lymph nodes and the spleen. In addition, CHR treatment decreased CD80 and CD86 expression markers of splenic CD11c+ cells and decreased NF-κB expression in the colon and splenic CD11c+ cells. In vitro, CHR decreased CD40, CD80, CD86, IL-6, and IL-12p40 expression in naïve bone marrow-derived CD11c+ DC stimulated lipopolysaccharide. Using a pharmacological approach, we demonstrated the impact of CHR on the NF-κB pathway. In a clinical setting, 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, potentially through the regulation of DC-related markers and CD11c+ cells.
Although we have demonstrated that CHR may have a potential therapeutic interest, additional markers and detailed mechanisms of action need to be determined in a large sample.