Biomedical subjects

Makoto Itoh

Publications and source records attributed to Makoto Itoh.

At least 19 recordsLinked to original sources

PubMed2006

Pharmacokinetic study of pleural fluid penetration of carbapenem antibiotic agents in chemical pleurisy.

STUDY OBJECTIVES: We investigated pleural fluid penetration of carbapenem antibiotic agents [imipenem (IPM), panipenem (PAPM), meropenem (MEPM), and biapenem (BIPM)] using an experimental rabbit pleuritis model to clarify the usefulness of the carbapenem agents for the treatment of bacterial pleurisy or pyothorax. MEASUREMENTS AND RESULTS: Serum and pleural fluid specimens were serially collected at 5, 10, 15, 30, 60, 90, 120, 180, 240, 300, and 360 min after antibiotic administration for measurement of antibiotic levels. We investigated each agent alone as well as drug solutions containing each agent and a dehydropeptidase-I-specific inhibitor, cilastatin (CS), to remove the influence of dehydropeptidase-I-related hydrolysis. Groups of animals (n=3) received each carbapenem agent with or without CS. Serum and pleural fluid antibiotic levels were measured by high-performance liquid chromatography (HPLC). Because Cmax is not useful for evaluating the antimicrobial effects of carbapenem antibiotic agents due to their dose-dependent antimicrobial activity, we also investigated the AUC, which is correlated with the total drug levels in vivo. Among the drug solutions containing CS, MEPM/CS had the highest pleural fluid AUC0-360 (1594.8+/-510.3 microg min/ml), and the highest pleural fluid AUC0-360/plasma AUC0-360 ratio (0.79+/-0.04). BIPM/CS had the highest plasma AUC0-360 (3040.1+/-1525.9 microg min/ml). In pleural fluid AUC0-360/plasma AUC0-360 ratio MEPM/CS was significantly higher than those for the remaining agents. In pleural fluid AUC0-360 and plasma AUC0-360 there were no significant differences among these mixed solutions. CONCLUSIONS: MEPM had the most favorable pleural fluid penetration. Pleural fluid penetration should be examined in infection models and in clinical trials.

Animals↗

PubMed2006

Blocking of protease allergens with inhibitors reduces allergic responses in allergic rhinitis and other allergic diseases.

CONCLUSIONS: Allergic responses specific to the corresponding proteases were reduced by protease inhibitors, suggesting promise as potent treatments for allergic rhinitis and other allergic conditions. OBJECTIVE: Allergic diseases, such as allergic rhinitis, are caused by the overproduction of IgE antibodies to various allergens. Many reported allergens are proteases that are cysteine, serine, aspartic (acid) proteases and metalloproteases. Conjugation of E64 inhibitor with cysteine protease allergens inhibits the IgE response to the same allergens. However, whether inhibitors of the other protease families reduce IgE levels and whether protease inhibitors reduce allergic symptoms remain controversial. Therefore, we compared the abilities of active and inhibitor-blocked inactive forms of proteases to generate IgE and allergic symptoms in this study to evaluate associations between the allergic response and protease inhibitors. MATERIALS AND METHODS: We measured levels of IgE, IgG1, IgG2a, and IgG2b enzyme-specific antibodies, and counted frequency of sneezing and nasal rubbing behavior in mice immunized with active or inactive forms of bromelain, chymotrypsin, chymosin and collagenase (a cysteine protease, a serine protease, an aspartic protease and a metalloprotease, respectively). RESULTS: All the inhibitors reduced IgE and IgG1 production in response to corresponding enzymes, and a cysteine protease inhibitor, E64, decreased nasal symptoms, such as sneezing and nasal rubbing.

Allergens↗

PubMed2006

[Clinical evaluation of covered self-expandable metallic stent for unresectable malignant stomach pyloric region and duodenal obstruction].

We evaluated palliative treatment for unresectable malignant stomach pyloric region and the duodenal obstruction using covered self-expandable metallic stent (SEMS). Fifty-seven patients (26 stomach pyloric stenosis, 31 duodenal stenosis) were underwent palliative treatment using covered SEMS. The covered SEMS was Ultraflex stent for esophageal obstruction. The covered SEMS was successfully indwelled in the target region in 56 patients. The patients became able to ingest orally after a mean of 2 days, and 96% of the patients (54/56) became able to eat solid or semi-solid diets later. The SEMS obstruction by tumor ingrowth or hyperplasia was not occurred, so SEMS was maintenance-free. We concluded covered SEMS was useful palliative treatment because it prevented SEMS obstruction by tumor ingrowth or hyperplasia and it was maintenance-free.

Aged↗

PubMed2005

Frequent c-Kit gene mutations not only in gastrointestinal stromal tumors but also in interstitial cells of Cajal in surrounding normal mucosa.

Gastrointestinal stromal tumors (GISTs) are thought to originate from mesenchymal stem cells that differentiate toward the interstitial cells of Cajal (ICCs). The frequent occurrence of activating mutations involving exon 11 of c-Kit gene in sporadic GISTs indicates an important role in genesis of this tumor type. In the present study we examined c-Kit gene mutations in a series of GISTs and also in ICCs of surrounding normal tissues. Samples from 18 patients were monitored immunohistochemically for c-Kit expression and microdissected for sequencing analysis of exons 9, 11, 13, and 17 of the c-Kit gene. It was revealed to be mutated in exon 11 or adjacent introns in 9 out of the total of 18 (50.0%) GISTs. In 6 (33.3%) cases, mutations in ICCs were also detected in the same exon. With stomach GISTs, 8 of 16 (50.0%) cases harbored mutations and 4 had mutations in background ICCs (25.0%). In contrast counterpart ICCs in gastric cancer cases harbored no c-Kit gene mutations (0 out of 24=0%) (P<0.02). ICCs undergoing c-Kit mutation as a possible early initiation step in GIST tumorigenesis may thus have pre-neoplastic potential.

Adult↗

PubMed2005

Combined effects of panipenem and aminoglycosides on methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa in vitro.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa are the main causes of refractory infections that are often resistant to antimicrobial agents. In these cases, combination of agents with antimicrobial activity is being examined. However, few studies have investigated combined effects with antimicrobial agents including carbapenem and aminoglycosides. METHODS: We evaluated the effects of panipenem (PAPM) combined with 3 aminoglycosides, arbekacin, amikacin, and netilmicin, and vancomicin (VCM) with an agar dilution checkerboard technique and the fractional inhibitory concentration index against 47 strains of MRSA and 56 strains of P. aeruginosa. RESULTS: PAPM combined with VCM achieved a synergic effect against MRSA in 80.9%. PAPM combined with aminoglycosides showed only additive effects against MRSA and P. aeruginosa. When comparing the activity of Mueller-Hinton agar (MHA) medium with MHA medium diluted 40-fold (1/40 MHA) against P. aeruginosa, the mean minimum inhibitory concentration of PAPM was decreased to 1/16. CONCLUSIONS: Combination of PAPM and VCM is effective against MRSA. Combinations of PAPM and aminoglycosides showed additive effects against MRSA and P. aeruginosa.

Aminoglycosides↗

PubMed2005

Increased gene expression of collagen Types I and III is inhibited by beta-receptor blockade in patients with dilated cardiomyopathy.

AIMS: To elucidate the cellular mechanisms of cardioprotection of beta-blockers in patients with heart failure, we investigated the effects of beta-blockers on collagen synthesis in patients with dilated cardiomyopathy (DCM). METHODS AND RESULTS: We examined the gene expression before and 4 months after the administration of a beta-blocker in 17 DCM patients. The messenger ribonucleic acid expression of collagen Types I and III (Col I and III) and transforming growth factor-beta(1) (TGF-beta(1)) of right ventricular tissues obtained by the endomyocardial biopsy were assessed by quantitative reverse transcriptase-polymerase chain reaction. Cardiac sympathetic nerve activity was assessed by the washout rate (WR) of (123)I-metaiodobenzylguanidine from the heart. Left ventricular ejection fraction (21 +/- 7 vs. 35 +/- 9%) and WR (53+/-14 vs. 42 +/- 13%) improved significantly. Before the beta-blocker treatment, the expressions of both Col I (r = 0.560, P = 0.041) and Col III (r = 0.630, P = 0.008) genes were correlated with WR. The expression levels of both Col I (1.08 +/- 0.72 vs. 0.65 +/- 0.26, P = 0.024) and Col III (2.06 +/- 1.81 vs. 1.05 +/- 0.74, P = 0.018) were reduced by a beta-blocker. Changes in TGF-beta(1) correlated with those in WR (r = 0.606, P = 0.002). CONCLUSION: beta-Blockers are considered to inhibit the expression of collagen-related genes in DCM, which seems to be mediated by TGF-beta(1).

Adrenergic beta-Antagonists↗

PubMed2005

IL-8 promotes cell proliferation and migration through metalloproteinase-cleavage proHB-EGF in human colon carcinoma cells.

Interleukin-8 (IL-8) has been reported to promote tumor cell growth in colon cancer cells after binding to its receptors, which are members of the G-protein coupled receptor (GPCR) family. Recent studies demonstrated that stimulation of GPCR can induce shedding of epidermal growth factor (EGF) ligands via activation of a disintegrin and metalloprotease (ADAM), with subsequent transactivation of the EGF receptor (EGFR). In this study, we investigated mechanisms of cell proliferation and migration stimulated by IL-8 in a human colon carcinoma cell line (Caco2). IL-8 increased DNA synthesis of Caco2 in a dose dependent manner and this was inhibited by ADAM, EGFR kinase, and MEK inhibitors. IL-8 transiently induced EGFR tyrosine phosphorylation after 5-90 min and this was completely inhibited by ADAM inhibitor. Neutralizing antibody against HB-EGF as a key ligand for EGFR also blocked transactivation of EGFR and cell proliferation by IL-8. Since IL-8-induced cell migration was further suppressed by the ADAM inhibitor and the HB-EGF neutralizing antibody, our data indicate that IL-8 induces cell proliferation and migration by an ADAM-dependent pathway, and that HB-EGF plays an important role as the major ligand for this pathway.

Caco-2 Cells↗

PubMed2005

Troglitazone, a PPAR-gamma activator prevents endothelial cell adhesion molecule expression and lymphocyte adhesion mediated by TNF-alpha.

BACKGROUND: Cytokine mediated induction of the mucosal addressin cell adhesion molecule-1(MAdCAM-1) expression is associated with the onset and progression of inflammatory bowel disease (IBD). RESULTS: Using western blotting and cell-based ELISA, we show in this study that troglitazone, an activator of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma), widely used in the treatment of diabetes, has as well recently been highlighted as protective in models of inflammation and cancer. We found that troglitazone (10-40 microM), significantly reduced the TNF-alpha (1 ng/ml) mediated induction of endothelial MAdCAM-1 in a dose-dependent manner, achieving a 34.7% to 98.4% reduction in induced MAdCAM-1. Trogliazone (20 microM) reduced TNF-alpha induced VCAM-1, ICAM-1 and E-selectin expression. Moreover, troglitazone significantly reduced alpha4beta7-integrin dependent lymphocyte adhesion to TNF-alpha cultured endothelial cells. CONCLUSIONS: These results suggest that PPAR-gamma agonists like troglitazone may be useful in the clinical treatment of IBD.

Animals↗

PubMed2005

C-reactive protein elevation predicts the occurrence of atrial structural remodeling in patients with paroxysmal atrial fibrillation.

It has been poorly understood whether inflammation may contribute to atrial structural remodeling and increase the propensity for atrial fibrillation (AF) to persist. We investigated the relationship between C-reactive protein (CRP) elevation and the development of atrial remodeling in AF. The study population comprised 50 consecutive paroxysmal AF (PAF) patients and 50 control patients without AF. All patients underwent echocardiography, and high-sensitivity CRP was routinely measured. C-Reactive protein was significantly higher in the patients with PAF than control patients (0.231+/-0.176 mg/dl vs 0.055+/-0.041 mg/dl, P<0.001). Other predictors of elevated CRP included left ventricular mass (P<0.05), left ventricular end-systolic diameter (P<0.05), and left atrial (LA) diameter (P<0.001). In a multivariate analysis, only CRP and LA diameter were independent predictors of PAF. Elevated CRP levels correlated with LA diameter (r=0.489, P<0.001). Left atrial diameter was increased in PAF patients compared with control patients (P<0.001). We found that a longer duration of AF is associated with higher CRP levels and a larger LA diameter (duration <30 days: CRP 0.166+/-0.139 mg/dl, LA diameter 38.4+/-8.0 mm; duration >30 days: CRP 0.345+/-0.181 mg/dl, LA diameter 45.6+/-6.6 mm; P<0.001). In conclusion, longer AF duration is associated with CRP elevation and atrial structural remodeling, as approximated by larger LA diameter. However, CRP elevation, while correlating with LA diameter, was not an independent predictor of atrial structural remodeling. Thus, it remains unclear whether CRP and the inflammatory state are contributory to LA remodeling or whether LA remodeling or AF induces elevation in CRP and inflammation.

Aged↗

PubMed2005

Isolation of nontuberculous mycobacteria from patients with pneumoconiosis.

This study aimed to confirm the isolation of nontuberculous mycobacteria (NTM) from patients with pneumoconiosis. Monthly sputum examinations in 155 patients were performed from April 1998 to December 2002. When NTM were isolated, species were identified and the frequency of isolation was reviewed. We then identified the patients who satisfied the bacteriologic criteria for the diagnosis of nontuberculous mycobacterial pulmonary disease (NTM pulmonary disease) recommended by the American Thoracic Society (ATS). Symptoms and findings on computed tomography (CT) scans were evaluated. NTM were isolated from 60 patients (39%): common etiologic species defined by the ATS, i.e., Mycobacterium avium, M. intracellulare, M. abscessus, and M. kansasii, were identified in 21 patients; unusual etiologic species, i.e., M. fortuitum, M. simiae, and M. szulgai, were identified in 11 patients; and undefined species, which appeared to be nonpathogenic, were identified in 41 patients. The bacteriologic criteria were satisfied in 8 patients. NTM species isolated in conformity with the bacteriologic criteria were: M. avium in 4 patients, M. intracellulare in 2, a combination of M. intracellulare and M. kansasii in 1, and M. gordonae in 1 patient. Two patients, from whom M. avium were repeatedly isolated, satisfied the ATS diagnostic criteria for NTM pulmonary disease. It is important to note that NTM, including both pathogenic species and nonpathogenic species, were isolated from patients with pneumoconiosis.

Aged↗

PubMed2005

Helicobacter pylori-stimulated interleukin-8 (IL-8) promotes cell proliferation through transactivation of epidermal growth factor receptor (EGFR) by disintegrin and metalloproteinase (ADAM) activation.

Helicobacter pylori infection increases the risk of hyperplastic polyps and gastric cancer, but the mechanisms remain to be elucidated. H. pylori was recently shown to transactivate epidermal growth factor receptor (EGFR) through metalloprotease stimulation. The present study was designed to investigate the effect of interleukin-8 (IL-8) induced by H. pylori infection on EGFR transactivation and epithelial cell growth. H. pylori Sydney strain 1 (SS1) having wild-type cag(+)A was used. Phospho-EGFR assay was performed by immunoprecipitation using anti-human EGFR and anti-phosphotyrosine antibodies. DNA synthesis was evaluated by [3H]thymidine uptake using the human gastric cancer cell line, KATO III. H. pylori induced EGFR phosphorylation, and a disintegrin and metalloproteinase (ADAM) inhibitor, KB-R7785, completely suppressed EGFR phosphorylation. IL-8 also induced EGFR phosphorylation, while anti-IL-8 and anti-IL-8 receptor (CXCR1) neutralizing antibodies suppressed EGFR phosphorylation. [(3)H]Thymidine uptake analysis demonstrated that H. pylori increased DNA synthesis in gastric epithelial cells, and tyrosine kinase inhibitor, MEK inhibitor, and ADAM inhibitor suppressed the DNA synthesis induced by H. pylori. H. pylori-stimulated IL-8 accelerates processing of EGFR ligands through ADAM activation, and cleaved EGFR ligands bind and stimulate EGFR in paracrine and autocrine manners to induce cell proliferation. This may be one of the mechanisms of hyperplastic polyp and gastric cancer development in H. pylori-infected gastric mucosa.

ADAM Proteins↗

PubMed2005

Prognostic indicators estimated by (99m)Tc-GSA in acute liver damage.

A prognostic estimation formula of acute liver damage was evaluated by using clinical data and technetium-99m-diethylenetriaminepentaacetic acid-galactosyl-human serum albumin ((99m)Tc-GSA) scintigraphy in order to determine operability for orthotopic liver transplantation (OLT). Forty-six patients hospitalized for acute liver damage were divided into survival (n=35) and non-survival (n=11) groups. Univariate and multivariate analyses were used to identify significant factors that affected prognosis. Logistic regression analysis was performed to predict prognosis with effective factors. Ten independent factors with significant differences were identified and further analyzed for significance by logistic regression analysis. Among the 10 factors, age and LHL15/HH15 were identified as having meaningful differences for predicting convalescence. The following formula was developed: A negative value for R indicates non-survivals, and a positive value indicates survivals. The mortality rate was calculated as=1/(1+e(R)). The sensitivity was 0.909, specificity was 1.000, and accuracy was 0.978. The reliability of this formula was as good as that of another formula presented previously by the Intractable Liver Diseases Study Group of Japan. The use of (99m)Tc-GSA for estimating the prognosis of acute liver damage is useful, especially before the onset of hepatic encephalopathy.

Journal Article↗

PubMed2005

Insulin enhances leukocyte-endothelial cell adhesion in the retinal microcirculation through surface expression of intercellular adhesion molecule-1.

The purpose of this study was to evaluate the effects of insulin on leukocyte-endothelial cell adhesion in the retinal microcirculation in vitro and in vivo. Human retinal endothelial cells (HRECs) were cultured in medium with or without insulin, and neutrophils allowed to adhere. Adherent neutrophils were quantified by measuring myeloperoxidase activity. Surface expression of endothelial adhesion molecules were studied with the use of an enzyme immunoassay. Insulin at concentrations of 50 and 100 microU/ml significantly increased neutrophil adhesion to HRECs compared with the control cells (P < 0.01, respectively). Surface expression of intercellular adhesion molecule-1 (ICAM-1) significantly increased when HRECs were exposed to 100 microU/ml insulin, as compared with the control cells (P < 0.05). Anti-ICAM-1 antibody significantly inhibited neutrophils adhesion to HRECs (P < 0.0001). Brown-Norway rats received subcutaneous injection of 0.2 U per 100 g body weight insulin three times. Control rats received the same amount of phosphate-buffered saline. Leukocyte entrapment in the retina was evaluated using acridine orange leukocyte fluorography. The number of leukocytes trapped in the retina of insulin-treated rats was significantly elevated compared with that in the control animals (P < 0.0001). These results suggested that insulin enhances leukostasis in retinal microcirculation. Hyperinsulinemia may be a risk factor of retinal microcirculatory disturbances.

Acridine Orange↗

PubMed2005

Bronchoscopic intralesional injection of triamcinolone acetonide treated against bronchial obstruction caused by peanut aspiration.

We encountered a case of obstructive pneumonia 1 month after peanut aspiration. Bronchoscopic examination revealed obstruction of the right basal bronchus with immature granulation tissue due to the peanut aspiration. Despite antibiotic treatment, the obstruction had not been resolved. To relieve the bronchial obstruction, bronchoscopic intralesional injection of triamcinolone acetonide was performed without any complications. Seven days after injection, the bronchial obstruction had resolve. In conclusion, intralesional injection of triamcinolone acetonide may play a role in one of the non-surgical repairs against obstruction due to foreign body aspiration.

Aged↗

PubMed2005

FTY720, an immunosuppressant, attenuates chronic pancreatitis in rats by suppressing T-cell infiltration.

OBJECTIVES: FTY720, a novel synthetic immunosuppressant, decreases peripheral blood lymphocytes by accelerating their homing to the peripheral and mesenteric lymph nodes and Peyer's patches. We previously reported that tacrolimus, another immunosuppressant, attenuates chronic pancreatitis by suppressing T-cell infiltration in male Wistar Bonn/Kobori rats but also may cause toxicity. To assess the effects of FTY720 on the development of pancreatic inflammation and fibrosis in the same model, the agent dissolved in physiologic saline was subcutaneously injected to 10-week-old male WBN/Kob rats for 10 weeks. METHODS: Parameters for inflammation and fibrosis were assessed and interferon-gamma and transforming growth factor-beta1 mRNA in the pancreas were determined by RT-PCR. RESULTS: Treatment with FTY720 attenuated gross alterations in the pancreas, including pigmentation and atrophy. This protective effect was quantitatively confirmed by significant increase in pancreatic weights and decreases in pancreatic myeloperoxidase activity (an index of granulocyte infiltration), pancreatic hydroxyproline content (an index of collagen deposition), ratio of fibrous tissue, and histologic scores. The obvious infiltration of CD4- and CD8-positive T cells into the pancreas in the saline group was almost completely prevented by administration of FTY720, which also suppressed overexpression of interferon and transforming growth factor-beta1 mRNA in the pancreas. CONCLUSION: We conclude that FTY720 prevents pancreatic inflammation and fibrosis by suppressing infiltration of CD4- and CD8-positive T cells and by downregulating induction of interferon and transforming growth factor-beta1 mRNA in the pancreas.

Animals↗

PubMed2005

53BP2 induces apoptosis through the mitochondrial death pathway.

The p53 binding protein 2 (53BP2) has been identified as the interacting protein to p53, Bcl-2, and p65 subunit of nuclear factor kappaB (NF-kappaB). The TP53BP2 gene encodes two splicing variants, 53BP2S and 53BP2L, previously known as apoptosis stimulating protein 2 of p53 (ASPP2). We found that these 53BP2 proteins are located predominantly in the cytoplasm and induce apoptosis as demonstrated by cleavage of poly ADP ribose polymerase (PARP) and annexin V staining. Furthermore, we demonstrate that 53BP2 is located in the mitochondria and induces apoptosis associated with depression of the mitochondrial trans-membrane potential (DeltaPsim) and activation of caspase-9. From these findings we conclude that 53BP2 induces apoptosis through the mitochondrial death pathway.

Apoptosis↗

PubMed2005

Intrahepatic biliary papilloma morphologically similar to biliary cystadenoma.

A 37-year-old man presented complaining of epigastralgia. Abdominal ultrasonography revealed the presence of a papillary tumor (9 mm in diameter) in the cystic lesion (18 mm in diameter) in hepatic segment 4, which was accompanied by mild intrahepatic bile duct dilatation. Although abdominal computed tomography also showed the cystic lesion, it did not show papillary tumors inside the lesion. Endoscopic retrograde cholangiography showed the communication between the cystic lesion and the left hepatic duct. In addition, mucus was observed in the common bile duct. When transpapillary intraductal ultrasonography was performed through the left hepatic duct using a fine ultrasonic probe, a hyperechoic papillary and lobulated tumor was clearly shown in the cystic lesion. The wall of the cyst was smooth and there was no sign of tumor infiltration. Based on these findings, biliary cystadenoma was diagnosed and an extended left lobectomy was carried out. However, pathological findings postoperatively revealed that the lesion was a localized biliary papilloma, developing and extending to the intrahepatic duct. This case is rare and there have been no published reports describing a biliary papilloma morphologically similar to biliary cystadenoma.

Adult↗

PubMed2005

Helicobacter pylori eradication decreases the expression of glycosylphosphatidylinositol-anchored complement regulators, decay-accelerating factor and homologous restriction factor 20, in human gastric epithelium.

BACKGROUND: It has previously been reported that there is a strong correlation between the expression of glycosylphosphatidylinositol (GPI)-anchored complement membrane inhibitor in gastric epithelium and the severity of inflammation of gastric mucosa. To investigate the regulation of complement activity in gastric epithelium during Helicobacter pylori (H. pylori)-associated gastritis, the expression of GPI-anchored complement membrane inhibitors, decay-accelerating factor (DAF) and 20-kDa homologous restriction factor 20 (HRF20), and membrane cofactor protein (MCP), which is a transmembrane protein, were evaluated after removal of the H. pylori stimulus. Furthermore, the expression of the complement fragment, C3c, was also investigated. METHODS: Forty-six patients with epigastric symptoms and endoscopically confirmed peptic ulcer or gastritis who had H. pylori infection of the gastric mucosa were enrolled in the present study. Biopsy specimens were obtained from the gastric antrum and corpus 1 month before and after eradication. Helicobacter pylori infection was determined by the rapid urease test, histology, and culture before eradication, and by histology, culture, and urea breath test after eradication. Gastric biopsy specimens obtained before and after eradication were evaluated for infiltration by neutrophils and mononuclear cells. The expression of complement membrane inhibitors, DAF, HRF20, and MCP and that of the main complement fragment, C3c, was immunohistochemically evaluated. RESULTS: One month after the eradication of H. pylori, the infiltration by neutrophils and mononuclear cells in the gastric mucosa decreased significantly (P < 0.0001) as compared with that before eradication. The expression of DAF, HRF20, and C3c on gastric mucosal epithelium also significantly decreased in both the antrum and the corpus (P < 0.05) 1 month after eradication. However, no change was observed in the expression of MCP. CONCLUSIONS: The decrease in the expression of GPI-anchored complement regulator and the complement after removal of a chronic microbial stimulus suggests that the gastric epithelium appears to undergo an aggressive stress of complement during H. pylori infection. Conclusively, DAF and HRF20 may play an important protective role against complement-mediated damage induced by chronic microbial stimuli in such a pathological condition.

Amoxicillin↗