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

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

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.
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*

Although Helicobacter pylori is susceptible to many antibiotics in vitro, only a few antibiotics, including amoxicillin, clarithromycin, metronidazole, tetracycline, and fluoroquinolones, have been frequently used in vivo to cure the infection in Korea. However, the frequent use for treatment regimens incorporating a proton pump inhibitor (PPI) and a combination of two or more antibiotics has resulted in the development of antibiotic resistance against H. pylori, which is a growing problem. The frequencies of resistance to antibiotics have varied widely according to geographical regions and subgroups within study populations. In this review article the prevalence of antibiotic resistance in H. pylori isolated from Korean patients, molecular mechanisms of the resistance and methods to detect the resistance have been discussed.
Amoxicillin ; Anti-Bacterial Agents ; Clarithromycin ; Drug Resistance, Microbial* ; Fluoroquinolones ; Helicobacter pylori* ; Helicobacter* ; Humans ; Korea ; Metronidazole ; Prevalence ; Proton Pumps ; Tetracycline

No abstract available.
Animals ; Gram-Negative Bacteria* ; Interleukin-2* ; Mice*

A complex microbiota colonizes mucosal layers in different regions of the human gut. In the healthy state, the microbial communities provide nutrients and energy to the host via fermentation of non-digestible dietary components in the large intestine. In contrast, they can play roles in inflammation and infection, including gastrointestinal diseases and metabolic syndrome such as obesity. However, because of the complexity of the microbial community, the functional connections between the enteric microbiota and metabolism are less well understood. Nevertheless, major progress has been made in defining dominant bacterial species, community profiles, and systemic characteristics that produce stable microbiota beneficial to health, and in identifying their roles in enteric metabolism. Through studies in both mice and humans, we are recently in a better position to understand what effect the enteric microbiota has on the metabolism by improving energy yield from food and modulating dietary components. Achieving better knowledge of this information may provide insights into new possibilities that reconstitution of enteric microbiota via diet can provide the maintenance of healthy state and therapeutic/preventive strategies against metabolic syndrome such as obesity. This review focuses on enteric microbial composition and metabolism on healthy and diseased states.
Animals ; Bacteria/growth & development/metabolism ; Diet ; Gastrointestinal Diseases/*microbiology/pathology ; Humans ; Inflammation/microbiology/pathology ; Intestines/microbiology ; Metabolic Syndrome X/*microbiology/pathology ; *Microbiota ; Probiotics