Abstract
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.
Highlights
Inflammatory bowel disease (IBD) is an umbrella term of chronic inflammatory disorders of the gastrointestinal tract [1]
Male Wistar rats (180–220 g) were randomly divided into two groups as detailed in [11]: the first group served as control, and the second group was induced by trinitrobenzene sulfonic acid (TNBS) based on the method described by Morris et al [12]
We used a rat model of TNBS-induced experimental colitis where inflammation develops in 72 h, in contrast, IBD is a chronic disease which often has very long duration
Summary
Inflammatory bowel disease (IBD) is an umbrella term of chronic inflammatory disorders of the gastrointestinal tract [1]. Previous studies described the effects of genetic alterations, environmental factors, life-style habits and the microbiome in the progression of IBD, but their independent examination may lead astray [4,5]. Characterization of gut flora of healthy individuals and IBD patients is currently a popular field of research, but it has not been ascertained yet whether the alteration of microbiome is the cause or the consequence of the disease [9,10]. Heterogeneity in the manifestation of symptoms, genetic background or the microbiome between individual patients obstruct the efficient determination of a general master regulator in this multilevel system
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