Anti-tumour activity of low-toxicity lipopolysaccharide of Bordetella pertussis

Ohnishi, Megumi; Kimura, Sadao; Yamazaki, Masatoshi; Oshima, Hiroki; Di, Mizuno; S, Abe; Yamaguchi, Hideyo

doi:10.1038/bjc.1994.204

Cited by 13 publications

(16 citation statements)

References 11 publications

(8 reference statements)

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“…5). Generally, LPS can activate or stimulate human MNC to enhance inflammatory immune reactions and antitumor immune responses in the host (24). However, it is noteworthy that H. pylori -derived LPS could not induce IL-12 or IFN-g production by the human MNC, although E. coli -derived LPS induced these cytokines remarkably (Fig.…”

Section: Discussionmentioning

confidence: 95%

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Helicobacter pyloriAugments Growth of Gastric Cancers via the Lipopolysaccharide-Toll-like Receptor 4 Pathway whereas Its Lipopolysaccharide Attenuates Antitumor Activities of Human Mononuclear Cells

Chochi¹,

Ichikura²,

Kinoshita

et al. 2008

Clinical Cancer Research

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Purpose: Helicobacter pylori is reportedly involved in the development of gastric cancer. We investigated the mechanisms by which H. pylori affects gastric cancer growth and antitumor immunities in the host, focusing on H. pylori^derived lipopolysaccharide (LPS). Experimental Design: H. pylori and four gastric cancer cell lines (MKN28, MKN45, NUGC3, and KATOIII) were used.We examined the effect of H. pylori or its LPS stimulationon cancer growth and the involvement of the H. pylori LPS-toll-like receptor 4 (TLR4) pathway. We also examined the cytotoxicities of H. pylori/LPS^stimulatedhumanmononuclear cells (MNC) against gastric cancer cells and the effect of H. pylori LPS stimulation on cytokine production by MNC. Results: H. pylori, as well as its LPS, augmented the growth of gastric cancers, all of which expressed TLR4. Neutralization of TLR4 almost completely abrogated the H. pylori^induced proliferative activity of cancer cells. Escherichia coli LPS also augmented cancer growth via the LPS-TLR4 pathway. However, only H. pylori^derived LPS attenuated the cytotoxicity of MNC against gastric cancer cells. Stimulation with H. pylori/LPS also down-regulated perforin production in cancer cell^cocultured CD56 + natural killer cells. H. pylori LPS induced neither interleukin-12 nor IFN-g production by MNC, although E. coli LPS did induce production of both significantly. Nevertheless, interleukin-12 stimulation restored the IFN-g^producing capacity of H. pylori LPS^stimulated MNC. Conclusion: H. pylori augmented the growth of gastric cancers via the LPS-TLR4 pathway, whereas it attenuated the antitumor activity and IFN-g^mediated cellular immunity of MNC. H. pylori infection might thereby promote proliferation and progression of gastric cancers.

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Section: Discussionmentioning

confidence: 95%

“…Therefore, LPS derived from H. pylori may have certain influences on gastric cancer cells via TLR4. On the other hand, LPS is well known to have antitumor activity in experimental tumor-bearing animals (21)(22)(23)(24). LPS, in particular Escherichia coli -derived LPS, strongly activates macrophages to produce proinflammatory cytokines.…”

mentioning

confidence: 99%

Helicobacter pyloriAugments Growth of Gastric Cancers via the Lipopolysaccharide-Toll-like Receptor 4 Pathway whereas Its Lipopolysaccharide Attenuates Antitumor Activities of Human Mononuclear Cells

Chochi¹,

Ichikura²,

Kinoshita

et al. 2008

Clinical Cancer Research

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“…At this point, we consider as follows: The immunological mechanism may be related to inhibition of MM 46-tumor growth, because MM 46 carcinoma in C3H/He mice is moderately antigenic, 25) and its growth can be inhibited without cytotoxicity by immuno-stimulating agents, including mushroom -D-glucans such as lentinan 22,26) and PSK. [27][28][29] In this study, G. lucidum AF significantly countered the depression of splenic CD8 þ cells and protected against the decrease in IFN-and IL-4 production in regional lymph nodes in MM 46 tumor-bearing mice.…”

Section: Discussionmentioning

confidence: 99%

“…Syngeneic tumor model: 22) MM 46 mammary carcinoma (1 Â 10 6 cells) was inoculated i.p. into C3H/He mice.…”

Section: Methodsmentioning

confidence: 99%

Anti-Tumor Activities of the Antlered Form ofGanoderma lucidumin Allogeneic and Syngeneic Tumor-Bearing Mice

Nonaka

Shibata

Nakai

et al. 2006

Bioscience, Biotechnology, and Biochemistry

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“…In our preceding paper (15), we reported a new LPS isolated from Bordetella pertussis-killed vaccine (Tohama strain, BP-LPS) which has strong antitumor activity against MM46 mammary carcinoma, Meth A fibrosarcoma and MH134 hepatoma. This BP-LPS is less toxic than other LPS from enterobacteria such as Escherichia coli and Salmonella typhimurium.…”

mentioning

confidence: 99%

Characterization of Immunological Activity of a Low Toxicity Antitumor Lipopolysaccharide from Bordetella pertussis

Ohnishi

Kimura

Yamazaki

et al. 1994

Microbiology and Immunology

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Immunological properties of a low toxicity lipopolysaccharide (BP-LPS) extracted from Bordetella pertussis (Tohama strain) which was reported to have high antitumor activity against murine tumors were examined and compared with those of LPS extracted from other enterobacteria. The activation or stimulation of murine macrophages and lymphocytes by these LPS, including TNF induction, was found to be similar. However, BP-LPS was clearly less active in its stimulation of murine and human neutrophils as estimated by neutrophil-adherence assay and by their TNF production than E. coli LPS. Furthermore, BP-LPS also suppressed the activation of human neutrophils by Escherichia coli LPS. A comparative study with 7 LPS preparations indicated that their toxicity in terms of animal body weight loss correlated with their ability to induce human neutrophil adherence. The inability of BP-LPS to activate neutrophils may thus have some bearing on its low toxicity.

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Anti-tumour activity of low-toxicity lipopolysaccharide of Bordetella pertussis

Cited by 13 publications

References 11 publications

Helicobacter pyloriAugments Growth of Gastric Cancers via the Lipopolysaccharide-Toll-like Receptor 4 Pathway whereas Its Lipopolysaccharide Attenuates Antitumor Activities of Human Mononuclear Cells

Helicobacter pyloriAugments Growth of Gastric Cancers via the Lipopolysaccharide-Toll-like Receptor 4 Pathway whereas Its Lipopolysaccharide Attenuates Antitumor Activities of Human Mononuclear Cells

Anti-Tumor Activities of the Antlered Form ofGanoderma lucidumin Allogeneic and Syngeneic Tumor-Bearing Mice

Characterization of Immunological Activity of a Low Toxicity Antitumor Lipopolysaccharide from Bordetella pertussis

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