Lymphocyte infiltration and key differentially expressed genes in the ulcerative colitis

Abstract

Background: Ulcerative colitis (UC) was a type of inflammatory bowel diseases, which was difficult to cure and even would malignant turn into colon cancer. The specific etiology and molecular mechanism of UC were unclear to date. The purpose of this study was to search for new targets for the diagnosis and treatment of UC. Methods: Firstly, we downloaded the gene expression data of UC from the gene expression omnibus database database (GSE107499), and used multiple bioinformatics methods to find differently expressed genes (DEGs) in UC. Subsequently, we evaluated the lymphocyte infiltration in UC inflamed colon tissue by using the cell type identification by estimating relative subset of known RNA transcripts method. Results: We obtained 1175 DEGs and 8 hub genes (IL6, TNF, PTPRC, CXCL8, FN1, CD44, IL1B, and MMP9) in this study. Among them, 903 DEGs were up-regulated and 272 DEGs were down-regulated. Compared with non-inflamed colon tissues, the inflamed colon tissues had higher levels of memory B cells, activated memory CD4 + T cells, follicular helper T cells, M1 macrophages, resting dendritic cells, activated dendritic cells, activated mast cells, and neutrophils, whereas the proportions of plasma cells, resting memory CD4 + T cells, gamma delta T cells, activated NK cells, M2 macrophages and resting mast cells were relatively lower. Conclusions: The DEGs, hub genes and different lymphatic infiltration conditions can provide new targets for diagnosis and treatment of UC. However, these were just predictions through some theoretical methods, and more basic experiments will be needed to prove in the future.

Novel 3-strain Combinatorial Probiotics Alleviates Symptoms of Inflammatory Bowel Disease in Mice

“…The NLR and LMR were also restored significantly with WW-treatment, indicating a reduction in the inflammation (Figure 3B). In the colon and intestine, it has been seen that IBD leads to a higher proportion of memory B cells, activated CD4 + T cells, follicular helper T cells, M1 macrophages, dendritic cells (activated & resting), activated mast cells, and polymorphonuclear leukocytes [37]. The counts of CD45 + B220 + B cells, CD45 + CD3 + T cells, CD45 + CD3 + CD4 + T H cells, CD45 + CD3 + CD8 + T C cells, CD45 + GR1 + neutrophils, and CD45 + F4/80 + macrophages/monocytes in the Release of inflammatory mediators led to tissue degeneration, and subsequent loss in clonogenic potential, which was restored by WW, in the blood and colon (Figure 3F, 4H).…”

Dendritic cells: the yin and yang in disease progression

“…Atg16l1 autophagy gene deficiency promotes the bacterial translocation of DSS-induced colitis in vivo and regulates autophagy and phagocytosis, which lead to an exacerbation of the intestinal inflammation ( 119 ). The immune microenvironment of UC inflamed colon is composed not only by follicular Th cells and IL17A + Tregs, but also by memory cells (CD4 + T, IL17A + CD161 + T, and B cells), HLA-DR + CD56 + granulocytes, M1 macrophages, activated mast cells, neutrophils, and both resting and activated DCs ( 120 , 121 ). In CD patients, peripheral blood mononuclear cells have high expression of IL-1B in the Treg, DC and monocyte fractions ( 121 ), whereas the inflamed mucosa of those patients is characterized by IL-1B in HLA - DR + CD38 + T cells, TNF + IFN-γ + naïve B cells, and pDCs ( 121 ).…”

The role of B-lymphocytes and plasma cells in the pathogenesis of inflammatory bowel diseases

“…При встрече с антигеном и последующей активации, определяемой природой антигена, некоторая активация В-клеток происходит с помощью CD4+ Тh-клеток [Т-зависимая активация] и без помощи Тh-клеток [Т-независимая активация]; впоследствии В-лимфоциты могут не только дифференцироваться в плазматические клетки (ПК), но также и в B-клетки памяти [16], которые сами по себе вносят вклад в патогенез ЯК, поскольку они в большом количестве обнаруживаются в LP при этой патологии [17]. Хотя традиционно считалось, что единственной ролью ПК является секреция антител, но недавние исследования показали, что ПК сами могут ингибировать развитие фолликулярных Th -клеток, то есть эти Т-В-клеточные процессы здесь взаимосвязаны [16,18].…”