No abstract available.

No abstract available.
Epithelial Cells*

OBJECTIVE: Bacteroides fragilis, normal colonic inhabitant, is the most frequently isolated anaerobes in infected tissues, particularly in intraabdominal abscesses. In the acute infection model with abscesses, the response to B. fragilis infection is characterized by infiltration of neutrophils and macrophages. This study was designed to determine whether proinflammatory cytokines could be upregulated in peritoneal tissue of B. fragilis-infected mouse model. METHODS: After C57BL/6 mice were infected with abscess-inducing encapsulated B. fragilis, RNA was extracted from the intraperitoneal tissues. Cellular RNA was also extracted from mouse peritoneal macrophages (MPM) and human peripheral blood mononuclear cells (PBMC) after infection with B. fragilis. Expression of various cytokine mRNA was assessed using RT-PCR and standard RNA. Each cytokine protein was also measured by ELISA. RESULTS: B. fragilis-infected intraperitoneal tissues showed upregulated expression of IL-1u, IL-6 and TNFu mRNA. Expression of IL-1u and TNFu mRNA and protein was significantly higher in MPM or PBMC infected with B. fragilis than in those without infection. However, expression of IL-6 mRNA and protein was not increased in MPM or PBMC infected with B. fragilis compared with those without infection. CONCLUSION: These results suggest that the cytokines can be involved in immunopathologic reactions of the peritoneal tissue infected with B. jragilis.
Abscess ; Animals ; Bacteroides fragilis* ; Bacteroides* ; Colon ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-6 ; Macrophages ; Macrophages, Peritoneal ; Mice* ; Neutrophils ; RNA ; RNA, Messenger

Invasion of enteric bacteria, such as Salmonella and invasive E. coli, into intestinal epithelial cells induces proinflammatory gene responses and finally epithelial cell apoptosis. In this study, we asked whether invasive bacterial infection of human intestinal epithelial cells could upregulate cyclooxygenase-2 (COX-2) gene expression and whether increased COX-2 expression could influence intestinal epithelial cell apoptosis. Expression of COX-2 mRNA and prostaglandin (PG) E production were upregulated in HT-29 colon epithelial cells which were infected with S. dublin or invasive E. coli, as examined by quantitative RT-PCR and radioimmunoassay. Inhibition of COX-2 expression and PGE2 production using NS-398, a specific COX-2 inhibitor, showed a significant increase af epithelial cell apoptosis and caspase-3 activation in HT-29 cells infected with invasive bacteria. However, the addition of valerylsalicylate, a specific COX-1 inhibitor, did not change apoptosis in S. dublin-infected HT-29 cells. These results suggest that upregulated COX-2 expression and PGE2 production in response to invasive bacterial infection could contribute to host defense by inhibiting apoptosis of intestinal epithelial cells.
Apoptosis* ; Bacteria ; Bacterial Infections* ; Caspase 3 ; Colon ; Cyclooxygenase 2 ; Dinoprostone ; Enterobacteriaceae ; Epithelial Cells* ; Gene Expression ; HT29 Cells ; Humans ; Prostaglandin-Endoperoxide Synthases* ; Radioimmunoassay ; RNA, Messenger ; Salmonella

No abstract available.
Animals ; Interleukin-2* ; Lymphocytes* ; Rats* ; Shock*

No Abstract Available.
Bacteroides fragilis* ; Bacteroides* ; Chemokines, CXC* ; Enterotoxins* ; Epithelial Cells* ; Humans* ; NF-kappa B*

No Abstract Available.
Bacteroides fragilis* ; Bacteroides* ; Chemokines, CXC* ; Enterotoxins* ; Epithelial Cells* ; Humans* ; NF-kappa B*

No abstract available.

The distribution of minimal inhibitory concentrations (MIC) for amoxicillin, clarithromycin, metronidazole, tetracycline, azithromycin, and fluoroquinolone (ciprofloxacin, levofloxacin, and moxifloxacin) have shifted to higher concentrations from 1987 to 2003 in Helicobacter pylori (H. pylori) strains isolated from Korean patients. MIC values of secondary isolates were higher than those of primary isolates. Of treatment-failure patients, 16.4% showed mixed infections with both antibiotic-susceptible and -resistant H. pylori strains. A total of 89.6% of patients with treatment failure and 52.3% of patients without antibiotic treatment had H. pylori strains resistant to two or more antimicrobial agents (multi-drug resistance, MDR). The most common antibiotics showing MDR were clarithromycin, metronidazole, and azithromycin. The resistance rates to both amoxicillin and clarithromycin were 34.3% in secondary isolates and 6.2% in primary isolates. The resistance rates to both clarithromycin and metronidazole were 73.1% in secondary isolates and 7.7% in primary isolates. In addition, there was a significant difference in antibiotic resistance between two institutions located at Seoul and Gyeonggi provinces. To provide adequate informations about susceptible antibiotics to clinicians, continuous surveillance of antibiotic susceptibilities is needed in Korea.
*Drug Resistance, Bacterial ; Drug Resistance, Multiple, Bacterial ; Helicobacter pylori/*drug effects/isolation & purification ; Humans ; Korea ; Microbial Sensitivity Tests

Inflammatory bowel disease (IBD), the most important entities being ulcerative colitis and Crohn's disease, are chronic, relapsing and remitting inflammatory conditions that result from chronic dysregulation of the mucosal immune system in the intestinal tract. Although the precise pathogenesis of IBD is still incompletely understood, increased levels of proinflammatory cytokines, including interleukin (IL)-1beta, IL-18 and tumor necrosis factor-alpha, are detected in active IBD and correlate with the severity of inflammation, indicating that these cytokines may play a key role in the development of IBD. Recently, the intracellular nucleotide-binding oligomerization domain-like receptor (NLR) family members, including NLRP1, NLRP3, NLRC4 and NLRP6, are emerging as important regulators of intestinal homeostasis. Together, one of those aforementioned molecules or the DNA sensor absent in melanoma 2 (AIM2), apoptosis-associated speck-like protein containing 'a caspase recruitment domain (CARD)' (ASC) and caspase-1 form a large (>700 kDa) multi-protein complex called the inflammasome. Stimulation with specific microbial and endogenous molecules triggers inflammasome assembly and caspase-1 activation. Activated caspase-1 leads to the secretion of proinflammatory cytokines, including IL-1beta and IL-18, and the promotion of pyroptosis, a form of phagocyte cell death induced by bacterial pathogens, in an inflamed tissue. Therefore, inflammasomes are assumed to mediate host defense against microbial pathogens and gut homeostasis, so that their dysregulation might contribute to IBD pathogenesis. This review focuses on recent advances of the role of NLRP3 inflammasome signaling in IBD pathogenesis. Improving knowledge of the inflammasome could provide insights into potential therapeutic targets for patients with IBD.
CARD Signaling Adaptor Proteins/metabolism ; Carrier Proteins/metabolism/physiology ; Caspase 1/metabolism ; Humans ; Inflammasomes/*metabolism ; Inflammatory Bowel Diseases/metabolism/*pathology ; Interleukin-18/metabolism ; Interleukin-1beta/metabolism ; Signal Transduction