The value of LYM-1 cells for examining vacuole formation and loss of cell viability induced by culture supernates of Helicobacter pylori

Wang, X. M.; Kojima, Toshichika; Satoh, Kazue; Taniguchi, Yukako; Tokumaru, Kenkichi; Saifuku, Koji; Seki, Masako; Kihira, Ken; Ido, Kenichi; Uchida, Jun; Ohmori, Chiemi; Takaoka, T; Kimura, Kôichi

doi:10.1099/00222615-46-8-705

Cited by 3 publications

(4 citation statements)

References 14 publications

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“…Closer examination revealed that treatment with 300 µg/ml of AE for 24 hours induced cytoplasmic vacuoles in both OVCAR3 and SW626 cells (Figures 2J, 2N, 2L, 2P). These morphologic changes suggest that cell death may be occurring since cell death is sometimes accompanied by vacuole formation [21]. Further experiments were performed using 300 µg/ml concentration of AE.…”

Section: Resultsmentioning

confidence: 99%

Emblica officinalis Extract Induces Autophagy and Inhibits Human Ovarian Cancer Cell Proliferation, Angiogenesis, Growth of Mouse Xenograft Tumors

Papasian

et al. 2013

PLoS ONE

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Patients with ovarian cancer (OC) may be treated with surgery, chemotherapy and/or radiation therapy, although none of these strategies are very effective. Several plant-based natural products/dietary supplements, including extracts from Emblica officinalis (Amla), have demonstrated potent anti-neoplastic properties. In this study we determined that Amla extract (AE) has anti-proliferative effects on OC cells under both in vitro and in vivo conditions. We also determined the anti-proliferative effects one of the components of AE, quercetin, on OC cells under in vitro conditions. AE did not induce apoptotic cell death, but did significantly increase the expression of the autophagic proteins beclin1 and LC3B-II under in vitro conditions. Quercetin also increased the expression of the autophagic proteins beclin1 and LC3B-II under in vitro conditions. AE also significantly reduced the expression of several angiogenic genes, including hypoxia-inducible factor 1α (HIF-1α) in OVCAR3 cells. AE acted synergistically with cisplatin to reduce cell proliferation and increase expression of the autophagic proteins beclin1 and LC3B-II under in vitro conditions. AE also had anti-proliferative effects and induced the expression of the autophagic proteins beclin1 and LC3B-II in mouse xenograft tumors. Additionally, AE reduced endothelial cell antigen – CD31 positive blood vessels and HIF-1α expression in mouse xenograft tumors. Together, these studies indicate that AE inhibits OC cell growth both in vitro and in vivo possibly via inhibition of angiogenesis and activation of autophagy in OC. Thus AE may prove useful as an alternative or adjunct therapeutic approach in helping to fight OC.

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Section: Resultsmentioning

confidence: 99%

Emblica officinalis Extract Induces Autophagy and Inhibits Human Ovarian Cancer Cell Proliferation, Angiogenesis, Growth of Mouse Xenograft Tumors

Papasian

et al. 2013

PLoS ONE

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“…On the other hand, Cellini et al [21] showed that colonisation of mouse gastric mucosa by the helical form of H. pylori was induced by inoculation of the coccoid form. Wang et al [22] reported that both spiral and coccoid forms of H. pylori can cause acute gastritis and produce an antibody response in BALB/cA mice. The data obtained in the present study suggest that the coccoid form of H. pylori may also play some role in colonisation and induction of mucosal inflammation.…”

Section: Discussionmentioning

confidence: 99%

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

Osaki¹,

Yamaguchi²,

Taguchi³

et al. 2002

Journal of Medical Microbiology

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To determine the pathological significance of the coccoid form of Helicobacter pylori, its adhesion to and induction of secretion of interleukin-8 (IL-8) by gastric epithelial (MKN45) cells were studied. By flow cytometry, the adhesion of the coccoid form to MKN45 cells was significantly lower than that of the helical form. The monoclonal antibody A20 recognising lipopolysaccharide of H. pylori inhibited the adhesion of the coccoid form to MKN45 cells as much as that of the helical form. There was significantly lower induction of IL-8 secretion by MKN45 cells exposed to the coccoid form (two of four strains) as compared with the helical form.

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“…Whether there is any direct irreversible cytotoxic factor of H pylori remains to be determined. Although, so far, none of the studied factors met these requirements, there is some evidences that indicated cytoskeletal cell death or round-formed cell death differed from vacuolation-formed cell death [3,12,13] .…”

Section: Introductionmentioning

confidence: 95%

“…Irreversible degeneration and cell death were induced in gastric mucous epithelium infected with H pylori both in an in vitro and an in vivo study, including electron microscopic examination. These cells deteriorated without vacuolations, and biopsy specimens containing the organism obtained from gastric mucosa demonstrated a loss of microvilli and irreversible cell damage [1][2][3][4] . Even after eradication therapy of the bacterium, there were no significant differences in the histological scores and atrophic scores in the inflammation of the gastric body and the atrophy of the antrum [5][6][7][8][9] .…”

Section: Introductionmentioning

confidence: 99%