Interleukin-8 induction and adhesion of the coccoid form of Helicobacter pylori

Osaki, Takako; Yamaguchi, Hiroyuki; Taguchi, Haruhiko; Fukada, Minoru; Kawakami, Hayato; Honda, Hiroshi; Kamiya, Shigeru

doi:10.1099/0022-1317-51-4-295

Cited by 10 publications

(6 citation statements)

References 20 publications

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“…As the known interaction of DFMO with host cells prevents discrimination of the effect of DFMO on bacteria in the stomach we performed in vitro experiments using the human gastric AGS cell line in the absence of DFMO in the cocultures and observed that IL-8 expression was significantly reduced. Some studies using coccoid-form bacteria have reported that they induce lower levels of IL-8 in epithelial cells, and, concomitantly, adhere to a lesser degree than helical H. pylori [44], [45]. Our data indicate no loss of adherence of DFMO-treated bacteria, suggesting that other alterations of bacterial physiology are responsible for the reduction in IL-8 expression.…”

Section: Discussionsupporting

confidence: 56%

“…Some studies have reported that coccoid-form H. pylori exhibit reduced adherence compared to helical-shaped bacteria and that this correlates with lesser induction of IL-8 [44], [45]. To determine if a similar effect occurred with the bacteria altered by DFMO, we compared adherence to AGS cells of H. pylori grown with or without 1% DFMO for 12 h. There was not a decrease, but rather there was a modest increase in adherence, with 1.01±0.22% of untreated bacteria and 1.75±0.33% of DFMO-treated bacteria found to be adherent, respectively (Figure 7C).…”

Section: Resultsmentioning

confidence: 99%

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Difluoromethylornithine Is a Novel Inhibitor of Helicobacter pylori Growth, CagA Translocation, and Interleukin-8 Induction

et al. 2011

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Helicobacter pylori infects half the world's population, and carriage is lifelong without antibiotic therapy. Current regimens prescribed to prevent infection-associated diseases such as gastroduodenal ulcers and gastric cancer can be thwarted by antibiotic resistance. We reported that administration of 1% d,l-α-difluoromethylornithine (DFMO) to mice infected with H. pylori reduces gastritis and colonization, which we attributed to enhanced host immune response due to inhibition of macrophage ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis. Although no ODC has been identified in any H. pylori genome, we sought to determine if DFMO has direct effects on the bacterium. We found that DFMO significantly reduced the growth rate of H. pylori in a polyamine-independent manner. Two other Gram-negative pathogens possessing ODC, Escherichia coli and Citrobacter rodentium, were resistant to the DFMO effect. The effect of DFMO on H. pylori required continuous exposure to the drug and was reversible when removed, with recovery of growth rate in vitro and the ability to colonize mice. H. pylori exposed to DFMO were significantly shorter in length than those untreated and they contained greater internal levels of ATP, suggesting severe effects on bacterial metabolism. DFMO inhibited expression of the H. pylori virulence factor cytotoxin associated gene A, and its translocation and phosphorylation in gastric epithelial cells, which was associated with a reduction in interleukin-8 expression. These findings suggest that DFMO has effects on H. pylori that may contribute to its effectiveness in reducing gastritis and colonization and may be a useful addition to anti-H. pylori therapies.

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Section: Discussionsupporting

confidence: 56%

Section: Resultsmentioning

confidence: 99%

Difluoromethylornithine Is a Novel Inhibitor of Helicobacter pylori Growth, CagA Translocation, and Interleukin-8 Induction

et al. 2011

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“…4A). Cole et al (1997) and Osaki et al (2002) have shown that coccoid H. pylori have a reduced ability to induce IL-8 secretion compared with spiral H. pylori in AGS and KATO cells. The present study has also shown that the geneexpression level of IL-8 in GES-1 cells infected with coccoid H. pylori is lower than that of cells infected with spiral H. pylori.…”

Section: Adhesion Of Spiral and Coccoid H Pylori To Ges-1 Cellsmentioning

confidence: 99%

Gene-expression profiles in gastric epithelial cells stimulated with spiral and coccoid Helicobacter pylori

Liu

Chen

Tang³

et al. 2006

Journal of Medical Microbiology

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Human gastric epithelial immortalized GES-1 cells were infected with spiral and coccoid Helicobacter pylori. Scanning electron microscopy was used to determine the ability of the two forms of H. pylori to adhere to GES-1 cells. GES-1 cell apoptosis induced by coccoid and spiral H. pylori was analysed using flow cytometry. A cDNA microarray for 22 000 human genes was used to identify the gene-expression differences in GES-1 cells infected with the two forms of H. pylori, and the gene expression identified by the cDNA microarray was confirmed by RT-PCR. Scanning electron microscope observation showed that both coccoid and spiral bacteria can adhere to GES-1 cells. After 4 h infection, apoptosis induction was 27?4 % for spiral-form infection and 10?2 % for coccoid-form infection. Of 268 differentially expressed genes identified by cDNA microarray, 166 showed higher expression with the spiral H. pylori infection than with the coccoid H. pylori infection. To the best of the authors' knowledge, this is the first report that GES-1 cells infected with spiral H. pylori have higher expression of cxcl10, ccl11, ccl5, groa, TLR5, ATF3, fos, fosl2, gadd45a and myc. The cells infected with coccoid H. pylori had higher expression of survivin. The global profile of gene expression in GES-1 cells infected with coccoid and spiral H. pylori is described for the first time. INTRODUCTIONHelicobacter pylori is a prevalent Gram-negative microaerophilic bacterium that infects human gastric mucosa and causes many digestive diseases, such as chronic gastritis, peptic ulcers and gastric cancer (Nomura et al., 1991;Parsonnet et al., 1991; Graham et al., 1992). H. pylori exists in two morphological forms: an actively dividing spiral form and a non-culturable but viable coccoid form (Bode et al., 1993). Spiral H. pylori converts to the coccoid form under various unfavourable conditions, such as extended incubation (Catrenich & Maki, 1991;Reynolds & Penn, 1994), antibiotic treatment (Bode et al., 1993), nutrient deprivation (Mizoguchi et al., 1999), increased oxygen tension (Catrenich & Maki, 1991;Cellini et al., 1994), increased temperature (Shahamat et al., 1993), aerobic culture and alkaline pH (Cellini et al., 1994). Many researchers think that this morphological change may be a transitory adaptation to a particular environment as a means of species preservation, and that it may play an important role in antibiotic resistance and make the bacterium more difficult to eradicate. Also, the coccoid form might lead to difficult recovery, easy relapse and epidemic transmission (Mizoguchi et al., 1998). The spiral bacteria are the most common form found in the human stomach, but the coccoid bacteria are observed in more severely damaged regions of the gastric mucosa (Saito et al., 2003;Chan et al., 1994; Janas et al., 1995). Several reports have shown that although the coccoid form is non-culturable, it may be viable, as transcription and translation may actively take place in coccoid cells (Sisto et al., 2000;Monstein & Jonasson, 2001;Ng et al....

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“…Coccoid H. pylori is characterized by low virulence (including changes in cell adhesion, urease enzyme activity, cellular vacuolating cytotoxin, etc.) and a weak inflammatory response; therefore, it cannot be removed easily . H. pylori that presents in gastric cancer is usually in the coccoid form, and the coccoid H. pylori detection rate in gastric cancer tissue is significantly higher than that of in ulceration .…”

Section: Introductionmentioning

confidence: 99%

Proliferative and apoptotic effects of gastric epithelial cells induced by coccoid Helicobacter pylori

Han

Chen

et al. 2012

J. Basic Microbiol.

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Helicobacter pylori exhibit morphology convertion in a spiral or coccoid form. This study aims to reveal the impact of coccoid H. pylori on the proliferation and apoptosis of gastric epithelial cells. The cagA and vacA genes of H. pylori were detected by semi-quantitative RT-PCR. Proliferation and apoptosis were analyzed by the CCK-8 colorimetric method and TUNEL assay, respectively. Egr-1 mRNA and PCNA expression affected by the ERK1/2-specific inhibitor were detected by RT-PCR and immunochemistry. At low density of infection (MOI < 125:1), coccoid H. pylori exerted a stronger effect on proliferation and a weaker effect on apoptosis than did spiral form. The ERK1/2-specific inhibitor significantly blocked the increased expression in Egr-1 and PCNA induced by coccoid H. pylori. Expression of vacA and cagA in coccoid H. pylori decreased compared with the spiral form, whereas vacA decreased more than cagA. The difference of proliferation and apoptosis may be related to the unequal decreased expression of vacA and cagA in coccoid H. pylori. Activation of the ERK1/2-Egr-1-PCNA signal transduction pathway may play an important role in coccoid H. pylori-induced cell proliferation. Long latency of the coccoid form of H. pylori in gastric tissue may be associated with gastric cancer caused by H. pylori.

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Interleukin-8 induction and adhesion of the coccoid form of Helicobacter pylori

Cited by 10 publications

References 20 publications

Difluoromethylornithine Is a Novel Inhibitor of Helicobacter pylori Growth, CagA Translocation, and Interleukin-8 Induction

Difluoromethylornithine Is a Novel Inhibitor of Helicobacter pylori Growth, CagA Translocation, and Interleukin-8 Induction

Gene-expression profiles in gastric epithelial cells stimulated with spiral and coccoid Helicobacter pylori

Proliferative and apoptotic effects of gastric epithelial cells induced by coccoid Helicobacter pylori

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