Abstract
In the last two decades anti‐tumor necrosis factor (anti‐TNF) therapy for inflammatory bowel disease (IBD) has been widely used to induce and maintain clinical and endoscopical remission, completely changing management of the disease. In this study, we aimed to identify gene expression changes in inflamed mucosa from Crohn's disease and ulcerative colitis patients treated with 5‐aminosalicylic acid (5‐ASA) (N = 25) or anti‐TNF agents (N = 12) compared to drug‐free IBD patients (N = 12) and non‐IBD control subjects (N = 18). The mucosal expression of 84 genes previously associated with IBD was evaluated by qPCR. We found that both therapeutic regimens induce a decrease in LCN2, NOS2, and TFF1, the levels of which are overexpressed in drug‐free patients compared to non‐IBD control subjects. Interestingly, a stronger effect of anti‐TNF drugs was observed on LCN2 and TFF1 levels. However, 5‐ASA seems to induce a more robust reduction of NOS2 expression. Moreover, we found that anti‐TNF treatment significantly increased ABCB1, leading to levels similar to those found in non‐IBD control subjects.
Highlights
Inflammatory bowel diseases (IBDs) are chronic inflammatory conditions comprising Crohn's disease (CD) and ulcerative colitis (UC)
We used a target gene expression approach to examine genes implicated in inflammation, apoptosis, immune response, cellular adhesion, and tissue remodeling in order to assess changes in the colonic mucosa from IBD patients under different therapeutic regimens
Our findings showed that both 5-aminosalicylic acid (5-ASA) and anti-TNF agents are able to decrease the mucosal expression of LCN2, NOS2, and TFF1, the levels of which are overexpressed in untreated patients compared to non-IBD controls
Summary
Inflammatory bowel diseases (IBDs) are chronic inflammatory conditions comprising Crohn's disease (CD) and ulcerative colitis (UC). Thiopurines, and aminosalicylates (5-ASA), which have been used to treat IBD for decades. Limited use of corticosteroids due to severe adverse effects and biological advancements has created the premises for anti-TNF therapy. In the last two decades, apart from anti-tumor necrosis factor (anti-TNF) agents, other new therapeutic molecules targeting several immune pathways have been developed. The use of these drugs has improved longterm outcomes for both UC and CD (Reinisch et al, 2012; Schnitzler et al, 2009) with a significant increase in the economic burden on many national health care systems (Reinglas, Gonczi, Kurt, Bessissow, & Lakatos, 2018). If initially the therapeutic aim was to limit patient symptoms, current treatment goals for IBD include steroid-free remission, endoscopic healing, and lower surgery rates
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