Rapid Progression of Autoimmune Gastritis after Helicobacter pylori Eradication Therapy.

We herein report a case of autoimmune gastritis (AIG) with rapid progression after Helicobacter pylori eradication therapy. The patient's previous gastritis had followed the course of type B gastritis before eradication therapy for many years. Immediately after eradication, we diagnosed her with AIG and carefully followed changes in the endoscopic and histopathological findings and serum markers. All of these clinical findings showed significant atrophic progression in the corporal area for approximately three years. We concluded that H. pylori eradication therapy exacerbated AIG in this case.

Autoimmune Gastritis with a Long-term Course of Type B Gastritis: A Report of Two Cases.

Autoimmune gastritis (AIG) typically exhibits the characteristics of type A gastritis and has been classified as a separate disease from type B gastritis that corresponds to Helicobacter pylori gastritis. However, many reports have suggested the involvement of H. pylori infection in the pathogenesis of AIG. In our two cases, the patients' previous gastritis exhibited a clear pattern in which H. pylori gastritis had progressed over many years, but ultimately transitioned to AIG with its spontaneous disappearance. These findings suggest that some cases of AIG might originate from long-standing H. pylori gastritis.

alpha-Tomatine, the major saponin in tomato, induces programmed cell death mediated by reactive oxygen species in the fungal pathogen Fusarium oxysporum.

The tomato saponin alpha-tomatine has been proposed to kill sensitive cells by binding to cell membranes followed by leakage of cell components. However, details of the modes of action of the compound on fungal cells are poorly understood. In the present study, mechanisms involved in alpha-tomatine-induced cell death of fungi were examined using a filamentous pathogenic fungus Fusarium oxysporum. alpha-Tomatine-induced cell death of F. oxysporum (TICDF) occurred only under aerobic conditions and was blocked by the mitochondrial F(0)F(1)-ATPase inhibitor oligomycin, the caspase inhibitor D-VAD-fmk, and protein synthesis inhibitor cycloheximide. Fungal cells exposed to alpha-tomatine showed TUNEL-positive nuclei, depolarization of transmembrane potential of mitochondria, and reactive oxygen species (ROS) accumulation. These results suggest that TICDF occurs through a programmed cell death process in which mitochondria play a pivotal role. Pharmacological studies using inhibitors suggest that alpha-tomatine activates phosphotyrosine kinase and monomeric G-protein signaling pathways leading to Ca(2+) elevation and ROS burst in F. oxysporum cells.

Evaluation of calcium-alginate gel as an artificial diet medium for bioassays on common cutworms.

A calcium-alginate gel diet was developed for Spodoptera litura larvae, and its reliability as a carrier for incorporating antifeedants as well as insecticides was investigated. The alginate gel diet was prepared with a simple protocol, which does not involve any heating process. When tested using this diet, acephate, a Bacillus thuringiensis endotoxin formulation and rotenone reproducibly showed insecticidal activity against the larvae, while neem oil and scabequinone deterred the larval feeding effectively. However, not only the insecticidal activity of acephate but also the antifeedant activity of neem oil was reduced by replacing the alginate component by agar in the diet, suggesting the usefulness of the alginate gel diet as an assay tool for testing a broad range of samples against the larvae.

Alterations in the DNA binding activity of transcriptional factors activator protein-1, Sp1, and hepatocyte nuclear factor-1 in rat jejunum during starvation and refeeding.

BACKGROUND: The molecular processes leading to mucosal atrophy, regrowth, and functional changes with starvation and refeeding are largely unknown. There are many transcriptional factors that might be related to mucosal atrophy and proliferation. In contrast, we previously reported that H+/peptide transporter and aminopeptidase N messenger RNA in the intestinal mucosa were upregulated during starvation. Therefore, we selected and studied three transcriptional factors: activator protein (AP)-1, Sp1, and hepatocyte nuclear factor (HNF)-1, which not only play important roles for enterocytes proliferation, but also exist in promoter lesions of the brush border enzymes and peptide transporter. METHODS: In the present study, we performed electrophoretic mobility shift assays employing AP-1, Sp1, and HNF-1, and evaluated the changes in the DNA binding activities in rat jejunum during starvation and refeeding. RESULTS: Two days after starvation, the Sp1 binding activity was significantly decreased to 61.8% as compared with the control level, whereas AP-1 was 121.4% and HNF-1 was 77.5%. Two hours after refeeding, the AP-1 activity was significantly increased to 175.0% as compared with the control level, and the HNF-1 activity was significantly increased to 180.2%. In contrast, the decreased SP1 level did not recover until 24 h after refeeding. CONCLUSIONS: The DNA binding activities of these three transcriptional factors were significantly changed in the rat jejunum during starvation and refeeding. Our results provide insight into the molecular mechanisms of the transcriptional regulations associated with mucosal atrophy, regrowth, and functional changes of the jejunal epithelium in response to starvation and refeeding.

Mucosal permeability regulates receptor binding of luminal epidermal growth factor in the adult rat intestine.

Epidermal growth factor (EGF) stimulates repair in the damaged intestine, but its role in the normal intestine is not clear. Because EGF receptors are found on the basolateral surface but not the luminal surface, we hypothesized that mucosal permeability regulates EGF binding. Adult male rats were divided into 3 groups, one that was fed normal chow (the control), one that was starved for 4 days, and one that was given methotrexate (MTX) intragastrically (10 mg/kg/day for 3 days). The rats were sacrificed and everted sacks of the jejunum were made and incubated in EGF solution. Western blot analysis of mucosal homogenates showed that the amount of phosphotyrosyl EGF receptor in the starved and MTX-treated groups was, respectively, about 1.5 times and 2 times that in the control group. The mucosal permeability in the starved and MTX treated groups also increased and varied directly with the amount of phosphotyrosyl EGF receptor. These results suggest that in the adult rat intestine, luminal EGF may play a role only under tissue damage, where enhanced permeability permits the EGF to pass through the mucosa and bind to its receptor on the basolateral membrane.

Luminal polyamines upregulate transmural glucose transport in the rat small intestine.

BACKGROUND: Polyamines, which are contained in many foods, play an important role in the growth and differentiation of the enterocyte, but their role in glucose transport is unclear. Using isolated rat small intestine and a nonrecirculating perfusion system, we studied the effect of luminal polyamines on glucose uptake and on the concentration of sodium-glucose transporter 1 (SGLT1) and glucose transporter 5 (GLUT5) proteins. METHODS: In the control group, 300mg glucose solution was administered through the jejunum, and the glucose concentration in the portal vein was measured for 15 min. In treatment groups, various concentrations of polyamine (putrescine [Put] or spermine [Spm]) were administered simultaneously with the glucose. At the end of the perfusion period, the amount of SGLT1, GLUT5, and aminopeptidase N (APN) in the brush border membrane was subjected to Western blot analysis. RESULTS: Glucose concentration in the portal vein increased after the simultaneous administration of glucose and polyamines, and the area under the curve (AUC) after the 15-min perfusion was enhandced to 188%, 196%, 132%, and 192% by 0.5mM Spm, 4mM Spm, 1 mM Put, and 8 mM Put, respectively. The brush border membrane concentration of SGLT1 protein 15 min after polyamine administration was also enhanced in all treatment groups, and it correlated with the AUC. The concentration of GLUT5, on the other hand, was reduced by 4mM Spm, and the concentration of APN was not affected by polyamine administration. CONCLUSIONS: Luminal polyamines increase glucose absorption in the small intestine via the rapid enhancement of SGLT1 protein in the brush border membrane.