The purpose of this study is to assess the effects of anti-inflammatory on activation of nuclear factor-kappaB and mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in intestinal mucosal biopsy specimens from patients with ulcerative colitis (UC). A total of 27 cases with UC were investigated. 15 cases received sulfasalazine (SASP) treatment or SASP and glucocorticoid treatment, 12 cases did not receive any medication related with UC. Normal mucosa from 9 colon cancer cases served as control. Ten pieces of intestinal mucosal biopsy specimens were obtained from each patient. The mRNA expression of ICAM-1 and VCAM-1 were determined by reversal transcription-polymerase chain reaction (RT-PCR). The protein levels of ICAM-1 and VCAM-1 were measured by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay (EMSA). The results showed that NF-kappaB DNA binding activity, mRNA and protein expression of ICAM-1 and VCAM-1 were increased significantly in patients with UC, compared with normal control (P<0.05). Glucocorticoids and SASP markedly inhibited NF-kappaB activation and significantly decreased mRNA and protein expression of ICAM-1 and VCAM-1 (P<0.05). Adhesion molecules (ICAM-1 and VCAM-1) gene activation had significant positive correlation with the NF-kappaB DNA binding activity (r=0.8652 P<0.05, r=0.7902, P<0.05, respectively). We concluded that NF-kappaB is a major and essential factor in regulating the expression of adhesion molecules, it plays an important role in the pathogenesis of UC. SASP and glucocorticoids ameliorate UC via inhibition of NF-kappaB activation and reduction of adhesion molecules expression.
Adult ; Anti-Inflammatory Agents ; therapeutic use ; Colitis, Ulcerative ; drug therapy ; metabolism ; Female ; Humans ; Intercellular Adhesion Molecule-1 ; biosynthesis ; genetics ; Intestinal Mucosa ; metabolism ; Male ; NF-kappa B ; metabolism ; Prednisone ; therapeutic use ; RNA, Messenger ; biosynthesis ; genetics ; Sulfasalazine ; therapeutic use ; Vascular Cell Adhesion Molecule-1 ; biosynthesis ; genetics

Objective To investigate the distribution and drug resistance of pathogenic bacteria for infection after liver transplantation, and to provide a scientific basis for the rational clinical application of antibiotics. Methods The pathogenic bacteria isolated from the specimens of 904 patients with infection after liver transplantation in The Affiliated Hospital of Qingdao University from March 2014 to December 2021 were analyzed in terms of distribution and drug resistance. WHONET 5.6 software was used to perform a statistical analysis of strains and bacterial resistance rate, and Excel was used to analyze the sources of specimens, composition ratios, and distribution of pathogenic bacteria. Results A total of 2 208 non-repetitive pathogenic bacteria were isolated, mainly from the specimens of respiratory tract (31.25%), bile (22.28%), ascites (13.18%), blood (8.38%), and drainage fluid (4.62%). The top 10 pathogenic bacteria were Klebsiella pneumoniae subspecies (10.69%), Enterococcus faecium (10.42%), Escherichia coli (8.24%), Pseudomonas aeruginosa (8.24%), Staphylococcus epidermidis (8.06%), Acinetobacter baumannii (7.93%), Stenotrophomonas maltophilia (6.61%), Enterobacter cloacae (3.22%), Staphylococcus haemolyticus (3.08%), and Staphylococcus aureus (2.94%), accounting for 69.43% of the total pathogenic bacteria. Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Klebsiella pneumoniae subspecies, and Acinetobacter baumannii were the main pathogenic bacteria isolated from respiratory tract specimens; Enterococcus faecium was the main pathogenic bacterium isolated from bile, ascites, and drainage fluid specimens; Escherichia coli , Staphylococcus epidermidis , and Klebsiella pneumoniae subspecies were the main pathogenic bacteria isolated from blood specimens. Drug sensitivity data showed that Enterobacterales bacteria had a relatively high resistance rate to cephalosporins and fluoroquinolones and a resistance rate of < 10% to amikacin among aminoglycosides, with no strains resistant to tigecycline; compared with Escherichia coli , Klebsiella pneumoniae subspecies had a higher resistance rate to meropenem (14.71% vs 5.66%) and imipenem (11.35% vs 6.29%); non-fermentative bacteria had a relatively high resistance rate to carbapenems, with a resistance rate of < 10% to tigecycline and colistin. Among Gram-positive cocci, Enterococcus faecium had a resistance rate of 6.17% to vancomycin and 2.44% to quinupristin/dalfopristin, with no strains resistant to tigecycline and linezolid; Staphylococcus epidermidis had a resistance rate of > 50% to macrolides, fluoroquinolones, sulfonamides, and lincomycin, and a small part of these strains were resistant to linezolid and quinupristin/dalfopristin (< 3%), with no Staphylococcus epidermidis strains resistant to tigecycline and vancomycin. A total of 287 drug-resistant strains were monitored, accounting for 13%, among which there were 128 carbapenem-resistant Acinetobacter baumannii strains, 88 carbapenem-resistant Pseudomonas aeruginosa strains, 26 carbapenem-resistant Klebsiella pneumoniae subspecies strains, 11 carbapenem-resistant Escherichia coli strains, 23 methicillin-resistant Staphylococcus aureus strains, and 11 vancomycin-resistant Enterococcus strains. The carbapenem-resistant Klebsiella pneumoniae subspecies strains mainly produced serine carbapenemase, and the carbapenem-resistant Escherichia coli strains mainly produced metal β-lactamase. Conclusion Gram-negative bacteria are the main pathogenic bacteria for infection after liver transplantation, and there are differences in the distribution of pathogenic bacteria between different types of specimens. The resistance rate of some strains tend to increase, and therefore, it is necessary to strengthen the management of nosocomial infection and antibiotics.