The absence of Syndecan‐1 leads to more inflammation in the mouse model of inflammatory bowel disease (IBD)

Abstract

Introduction Inflammation of the gut lining constitute the basis for IBD pathogenesis, a disease with multifactorial etiology. In addition, there is suggestive evidence that the interaction of CD147, β1 integrin and Syndecan-1 (Sdc-1) could control the inflammation process and impact healing. Aim The aim of this work is to look at the pathogenesis of IBD in Sdc-1 null mice as compared to control (BALB/C). Our hypothesis is that in the absence of Sdc-1 a more severe inflammation will be observed. Method In this study, 32 male (16 BALB/c and 16 Sdc-1 null) mice, 8-10 weeks old were used after the Institutional Animal Care and Use Committee approval. They were divided equally into 4 groups. Half of the mice (8 BALB/C and 8 Sdc-1 null were given 1 cycle of 2.5 % DSS in drinking water for 1 week while the rest were given the 1st cycle of DSS then 2 weeks normal drinking water followed by a second cycle of 7 days of 2.5% DSS in drinking water. The animals were monitored and weighed daily/ observed clinically for body weight, stool consistency, gross bleeding scores as well as fecal occult blood. The animals were sacrificed at 1 week, 3 weeks and 4 weeks post DSS and 8 animals (4 BALB/C and 4 Sdc-1 null) were supposed to be sacrificed 6 weeks post DSS yet at week 5 all the Sdc-1null mice died while the BALB/C mice are still alive. The lengths of the colons were measured and the sigmoid part was used for histological comparison, at this stage, between the two strains. Results Preliminary data showed that in Sdc-1 null mice there was more weight loss, earlier rectal bleeding and death of animals compared to BALB/C. Moreover, the histological alterations in Sdc-1 null were more sever with more dissemination of the inflammation and cryptitis as well erosion of the intestinal lining epithelium compared to BALB/C mice. Conclusion Sdc-1null mice are more sensitive to IBD induction compared to the control BALB/C. The loss of Sdc-1 makes the inflammation more acute and lethal. More dose effect studies and characterizations are ongoing, hoping it will lead to a novel therapeutic approach for IBD treatment.