Chronic intestinal inflammation is characteristic of Inflammatory Bowel Disease (IBD)
that is associated with the exaggerated infiltration of immune cells. A complex interplay
of inflammatory mediators and different cell types in the colon are responsible for
the maintenance of tissue homeostasis and affect pathological conditions. Gene expression
alteration of colon biopsies from IBD patients and an in vivo rat model of colitis
were examined by RNA-Seq and QPCR, while we used in silico methods, such as Ingenuity
Pathway Analysis (IPA) application and the Immune Gene Signature (ImSig) package of
R, to interpret whole transcriptome data and estimate immune cell composition of colon
tissues. Transcriptome profiling of in vivo colitis model revealed the most significant
activation of signaling pathways responsible for leukocyte recruitment and diapedesis.
We observed significant alteration of genes related to glycosylation or sensing of
danger signals and pro- and anti-inflammatory cytokines and chemokines, as well as
adhesion molecules. We observed the elevated expression of genes that implies the
accumulation of monocytes, macrophages, neutrophils and B cells in the inflamed colon
tissue. In contrast, the rate of T-cells slightly decreased in the inflamed regions.
Interestingly, natural killer and plasma cells do not show enrichment upon colon inflammation.
In general, whole transcriptome analysis of the in vivo experimental model of colitis
with subsequent bioinformatics analysis provided a better understanding of the dynamic
changes in the colon tissue of IBD patients.