Background::The increasing incidence of inflammatory bowel disease (IBD) presents significant medical and societal challenges. A well-designed IBD database is crucial for both epidemiological studies and clinical management. However, inconsistencies between regional databases hinder cross-institutional and international research, especially between Eastern and Western societies.Methods::We developed a new IBD database, the 301 IBD database, integrating the IBD clinical characteristics from the Penn IBD database (USA) and the latest IBD guidelines and consensus and clinical practices of the Chinese PLA General Hospital (PLAGH). We applied this database to analyze clinical data of IBD inpatients at PLAGH from 2008 to 2023.Results::The 301 IBD database contains 490 items in 6 sections including demographic characteristics, personal history, clinical phenotype, disease activity, laboratory tests and examinations, and treatment. Features of the 301 IBD database include inpatient focus, biochemical indicators and opportunistic infection focus, and more about ulcerative colitis (UC)-associated complications. Single-center analysis revealed an increasing hospitalization trend, from 2.35% in 2008 to 3.94% in 2023. We found that the clinical characteristics of our UC inpatients are predominantly male (62.5%), extensive lesions (55.1%), low usage of biologics (4.1%), and a high incidence of UC-CRC (3.0%). The clinical characteristics of CD inpatients included male predominance (68.39%), early onset age (35.43 ± 14.75-year-old), and high rate of surgery (25.81%).Conclusion::The 301 IBD database, integrating Eastern and Western clinical data, provides a valuable tool for IBD clinical research. Future international, multicenter collaborations are expected to further enhance its utility.

Background::The increasing incidence of inflammatory bowel disease (IBD) presents significant medical and societal challenges. A well-designed IBD database is crucial for both epidemiological studies and clinical management. However, inconsistencies between regional databases hinder cross-institutional and international research, especially between Eastern and Western societies.Methods::We developed a new IBD database, the 301 IBD database, integrating the IBD clinical characteristics from the Penn IBD database (USA) and the latest IBD guidelines and consensus and clinical practices of the Chinese PLA General Hospital (PLAGH). We applied this database to analyze clinical data of IBD inpatients at PLAGH from 2008 to 2023.Results::The 301 IBD database contains 490 items in 6 sections including demographic characteristics, personal history, clinical phenotype, disease activity, laboratory tests and examinations, and treatment. Features of the 301 IBD database include inpatient focus, biochemical indicators and opportunistic infection focus, and more about ulcerative colitis (UC)-associated complications. Single-center analysis revealed an increasing hospitalization trend, from 2.35% in 2008 to 3.94% in 2023. We found that the clinical characteristics of our UC inpatients are predominantly male (62.5%), extensive lesions (55.1%), low usage of biologics (4.1%), and a high incidence of UC-CRC (3.0%). The clinical characteristics of CD inpatients included male predominance (68.39%), early onset age (35.43 ± 14.75-year-old), and high rate of surgery (25.81%).Conclusion::The 301 IBD database, integrating Eastern and Western clinical data, provides a valuable tool for IBD clinical research. Future international, multicenter collaborations are expected to further enhance its utility.

Objective: To investigate the effects of Helicobacter pylori (H.pylori) on the proliferation of GES-1 cells and the expressions of S100A8 and S100A9 in human gastric epithelial cell line GES-1. Methods: H. pylori were co-cultured with GES-1 cells at different infection plural (muhiplieity of infection (MOI) 50∶1, 100∶1, 200∶1), then the cells and cell culture supernatants were collected. The proliferative activity was detected by cell counting kit 8 (CCK-8) methods. The expression of S100A8 and S100A9 at mRNA level was determined by reverse transcription polymerase chain reaction (RT-PCR). The levels of S100A8 and S100A9 proteins and tumor necrosis factor-alpha (TNF-α) in cell culture supernatants were measured by enzyme linked immunosorbent assay (ELISA). T test and Pearson method were performed for statistical analysis. Results: The negative control group was taken as the baseline, the proliferation rates of GES-1 cells of the H. pylori multiplicity 50∶1 group, 100∶1 group and 200∶1 group were (105.51±4.78)%, (168.97±11.29)% and (64.05±10.11)%, respectively. There was no statistically significant difference in the proliferation rate of GES-1 cells between H. pylori multiplicity 50∶1 group and negative control group (t=0.69, P=0.51). The proliferation rate of GES-1 cells of the H. pylori multiplicity 100∶1 group was higher than that of the negative control group, and the difference was statistically significant (t=10.63, P<0.01). The proliferation rate of GES-1 in the H. pylori multiplicity 200∶1 group was lower than that of the negative control group, and the difference was statistically significant (t=-5.54, P<0.01). The expression of S100A8 and S100A9 at the mRNA level in the H. pylori multiplicity 200∶1 group was 0.31±0.21 and 8.66±4.08, respectively, which were higher than those of the negative control group (0.06±0.05 and 0.08±0.08), and the differences were statistically significant (t=10.20 and 6.89, both P<0.05). The expressions of S100A8 at the protein level of H. pylori multiplicity 50∶1, 100∶1, and 200∶1 groups were (112.21±1.25) ng/mL, (120.39±1.61) ng/mL and (121.28±0.71) ng/mL, respectively; while the expression of S100A9 at the protein level were (179.43±2.44) ng/mL, (191.47±1.98) ng/mL and (201.80±2.06) ng/mL, respectively; and the expression of TNF-α levels were (285.52±3.64) ng/mL, (320.08±2.28) ng/mL and (350.97±2.90) ng/mL, respectively; which were all higher than those of the negative control group ((76.14±1.30) ng/mL, (161.35±1.31) ng/mL and (270.08±2.96) ng/mL, respectively), and the differences were statistically significant (t_S100A8=35.09, 43.06, 43.92, t_S100A9 = 11.13, 18.54, 24.90, t_TNF-α= 6.34, 20.54, 33.23; all P<0.01). The expressions of S100A8 and S100A9 at the protein level were positively correlated with TNF-α (r=0.92 and 0.95, both P<0.01). Conclusion S100A8 and S100A9 may be involved in the process of H. pylori induced proliferation disorder and inflammation in GES-1 cells.