## 1 Introduction
In the course of UC, the polarization of naive T cells to Th2 cells stimulates the synthesis of proinflammatory cytokines such as IL-4, IL-13, and TNF-\(\alpha\). The observed differences in cytokine profiles between the diseases indicate a potential role of IL-12, as a biomarker used in differentiatingCD from UC. Despite the observed upregulation of TNF-\(\alpha\) in both [PERSON]'s disease and ulcerative colitis, the cellular sources of TNF-\(\alpha\) and the local profile of other cytokines are divergent. Therefore, the level of TNF-\(\alpha\), as well as its influence on immune cells and the development of the inflammatory response, differs between CD and UC, suggesting the potential utility of this parameter in the diagnosis of the diseases. The precise differences in TNF-\(\alpha\) action during the development of CD and UC are not clear; however, TNF-\(\alpha\) is able to induce the proinflammatory pathways such as nuclear factor \(\kappa\) B (NF-\(\kappa\)B) or mitogen-associated protein kinase (MAPK), resulting in the synthesis of other cytokines and chemokines like CCL2 (also known as monocyte chemoattractant protein-1, MCP-1). CCL-2 plays an important role in CD and UC as it recruits the monocytes, which are cells with a significant contribution to the pathogenesis of the diseases, to the inflammatory site and participates in the polarization of naive T cells to Th2 cells, being a phenotype characteristic for UC. Regarding the influence of CCL-2 on the immune cells, the serum profile of this biomarker might be useful in differentiating UC from CD [6; 7; 8; 9]. The development of the inflammatory process is also related to the alterations of endothelial cells, which, upon inflammatory triggers, express the adhesion molecules such as E- and P-selectin. E-selectin is exclusively expressed on the surface of endothelial cells, where it binds to the neutrophils, as well as to monocytes, basophils, and T cells. The expression of E-selectin on the cell surface occurs in the early stage of inflammation in response to IL-1 and TNF-\(\alpha\). Another adhesive molecule, P-selectin, is stored in the Weibel-Palade bodies of endothelial cells and in platelet granules. Factors triggering the release of P-selectin and its relocation to the cell membrane include histamine, thrombin, and TNF-\(\alpha\). The ligands for P-selectin are located on the surface of leukocytes and platelets; hence, the circulating level of P-selectin may not only reflect the activity of the inflammatory process, but also the activity of platelets, identifying the risk of thrombotic events [10; 11; 12]. One of the mediators of leukocyte-endothelial adhesion is IL-1\(\alpha\), which enhances the expression of vascular cell adhesion molecule-1 on endothelial cells. IL-1\(\alpha\) can act as a transcription factor but can also be expressed on the surface of numerous cells, including endothelial cells and epithelial cells of the gastrointestinal tract. This cytokine fulfills the role of \"alarmin\" since, upon release from necrotic cells, it can initiate and propagate local inflammatory processes [13; 14]. Considering the contrast in the activation and recruitment of leukocytes, as well as potential differences in leukocyte-endothelial interactions between [PERSON]'s disease and ulcerative colitis, the assessment of adhesion molecules and their mediators in the serum of patients could be used in the differential diagnosis of the diseases. The aim of this study is to identify diagnostic methods that could be used in the differential diagnosis of [PERSON]'s disease and ulcerative colitis. Therefore, in this research, we analyzed the serum profile of proinflammatory markers related to the pathogenesis of the disease (IL-12, TNF-\(\alpha\), CCL-2, E-selectin, P-selectin, IL-1\(\alpha\)) in patients with CD and UC to assess their utility in the differential diagnosis of the diseases. Moreover, another aim of this study is to identify to usefulness of the introduced biomarkers in the evaluation of the disease activity.