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Article: In Situ Delivery and Production System (

Taniguchi, Shun'ichiro

2021 Volume 11, Issue 6

Abstract: To selectively and continuously produce anti-cancer molecules specifically in malignant tumors, we have established an in situ delivery and production system ( ...

Abstract	To selectively and continuously produce anti-cancer molecules specifically in malignant tumors, we have established an in situ delivery and production system (
Language	English
Publishing date	2021-06-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm11060566
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Article ; Online: In Situ Delivery and Production System ( i DPS) of Anti-Cancer Molecules with Gene-Engineered Bifidobacterium

Shun’ichiro Taniguchi

Journal of Personalized Medicine, Vol 11, Iss 566, p

2021 Volume 566

Abstract: To selectively and continuously produce anti-cancer molecules specifically in malignant tumors, we have established an in situ delivery and production system ( i DPS) with Bifidobacterium as a micro-factory of various anti-cancer agents. By focusing on ... ...

Abstract	To selectively and continuously produce anti-cancer molecules specifically in malignant tumors, we have established an in situ delivery and production system ( i DPS) with Bifidobacterium as a micro-factory of various anti-cancer agents. By focusing on the characteristic hypoxia in cancer tissue for a tumor-specific target, we employed a gene-engineered obligate anaerobic and non-pathogenic bacterium, Bifidobacterium , as a tool for systemic drug administration. This review presents and discusses the anti-tumor effects and safety of the i DPS production of numerous anti-cancer molecules and addresses the problems to be improved by directing attention mainly to the hallmark vasculature and so-called enhanced permeability and retention effect of tumors.
Keywords	solid cancer ; microenvironment ; hypoxia ; cancer therapy ; DDS ; anaerobic bacteria ; Medicine ; R
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Potentiated antitumor effects of APS001F/5-FC combined with anti-PD-1 antibody in a CT26 syngeneic mouse model.

Shioya, Koichiro / Matsumura, Tomio / Seki, Yuji / Shimizu, Hitomi / Nakamura, Takaaki / Taniguchi, Shun'ichiro

Bioscience, biotechnology, and biochemistry

2021 Volume 85, Issue 2, Page(s) 324–331

Abstract: APS001F is a strain of Bifidobacterium longum genetically engineered to express cytosine deaminase that converts 5-fluorocytosine (5-FC) to 5-fluorouracil. In the present study, antitumor effects of APS001F plus 5-FC (APS001F/5-FC) in combination with ... ...

Abstract	APS001F is a strain of Bifidobacterium longum genetically engineered to express cytosine deaminase that converts 5-fluorocytosine (5-FC) to 5-fluorouracil. In the present study, antitumor effects of APS001F plus 5-FC (APS001F/5-FC) in combination with anti-PD-1 monoclonal antibody were investigated using a CT26 syngeneic mouse model. Both of dosing of APS001F/5-FC before and after anti-PD-1 mAb in the combination dosing exhibited antitumor effects as well as prolonged survival over the nontreated control. The survival rate in the combination therapy significantly increased over the monotherapy with APS001F/5-FC and that with anti-PD-1 mAb. Regulatory T cells among CD4+ T cells in tumor decreased in the combination therapy, while the ratio of CD8+ T cells was maintained in all groups. Taken these results together, APS001F/5-FC not only demonstrates a direct antitumor activity, but also immunomodulatory effects once localized in the hypoxic region of the tumor, which allows anti-PD-1 mAb to exert potentiated antitumor effects.
MeSH term(s)	Animals ; Antibodies, Monoclonal/immunology ; Antineoplastic Agents/pharmacology ; Bifidobacterium longum/genetics ; Bifidobacterium longum/physiology ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Cell Line, Tumor ; Flucytosine/pharmacology ; Genetic Engineering ; Mice ; Programmed Cell Death 1 Receptor/immunology
Chemical Substances	Antibodies, Monoclonal ; Antineoplastic Agents ; Programmed Cell Death 1 Receptor ; Flucytosine (D83282DT06)
Language	English
Publishing date	2021-02-17
Publishing country	England
Document type	Journal Article
ZDB-ID	1106450-x
ISSN	1347-6947 ; 0916-8451
ISSN (online)	1347-6947
ISSN	0916-8451
DOI	10.1093/bbb/zbaa057
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Article ; Online: Activation of the inflammasome drives peritoneal deterioration in a mouse model of peritoneal fibrosis.

Kadoya, Hiroyuki / Hirano, Akira / Umeno, Reina / Kajimoto, Eriko / Iwakura, Tsukasa / Kondo, Megumi / Wada, Yoshihisa / Kidokoro, Kengo / Kishi, Seiji / Nagasu, Hajime / Sasaki, Tamaki / Taniguchi, Shun'ichiro / Takahashi, Masafumi / Kashihara, Naoki

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 9, Page(s) e23129

Abstract: During peritoneal dialysis (PD), the peritoneum is exposed to a bioincompatible dialysate, deteriorating the tissue and limiting the long-term effectiveness of PD. Peritoneal fibrosis is triggered by chronic inflammation induced by a variety of stimuli, ... ...

Abstract	During peritoneal dialysis (PD), the peritoneum is exposed to a bioincompatible dialysate, deteriorating the tissue and limiting the long-term effectiveness of PD. Peritoneal fibrosis is triggered by chronic inflammation induced by a variety of stimuli, including peritonitis. Exposure to PD fluid alters peritoneal macrophages phenotype. Inflammasome activation triggers chronic inflammation. First, it was determined whether inflammasome activation causes peritoneal deterioration. In the in vivo experiments, the increased expression of the inflammasome components, caspase-1 activity, and concomitant overproduction of IL-1β and IL-18 were observed in a mouse model of peritoneal fibrosis. ASC-positive and F4/80-positive cells colocalized in the subperitoneal mesothelial cell layer. These macrophages expressed high CD44 levels indicating that the CD44-positive macrophages contribute to developing peritoneal deterioration. Furthermore, intravital imaging of the peritoneal microvasculature demonstrated that the circulating CD44-positive leukocytes may contribute to peritoneal fibrosis. Bone marrow transplantation in ASC-deficient mice suppressed inflammasome activation, thereby attenuating peritoneal fibrosis in a high glucose-based PD solution-injected mouse model. Our results suggest inflammasome activation in CD44-positive macrophages may be involved in developing peritoneal fibrosis. The inflammasome-derived pro-inflammatory cytokines might therefore serve as new biomarkers for developing encapsulating peritoneal sclerosis.
MeSH term(s)	Animals ; Mice ; Peritoneum ; Peritoneal Fibrosis ; Inflammasomes ; Peritonitis ; Disease Models, Animal ; Inflammation
Chemical Substances	Inflammasomes
Language	English
Publishing date	2023-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202201777RRR
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Article ; Online: Tumor-Targeting Therapy Using Gene-Engineered Anaerobic-Nonpathogenic Bifidobacterium longum.

Taniguchi, Shun'ichiro / Shimatani, Yuko / Fujimori, Minoru

Methods in molecular biology (Clifton, N.J.)

2016 Volume 1409, Page(s) 49–60

Abstract: Despite great progress in molecular-targeting drugs for cancer treatment, there are problems of disease recurrence due to cancer-cell resistance to those drugs, derived from the heterogeneity of tumors. On one hand, the low-oxygen microenvironment ... ...

Abstract	Despite great progress in molecular-targeting drugs for cancer treatment, there are problems of disease recurrence due to cancer-cell resistance to those drugs, derived from the heterogeneity of tumors. On one hand, the low-oxygen microenvironment present in malignant tumor tissues has been regarded as a source of resistance of cancer cells against conventional therapie, such as radiation and chemotherapy. To overcome these problems, we have been developing a system to selectively deliver a large amount of anticancer drugs to malignant tumors by making use of the limiting factor, hypoxia, in tumors. Our strategy is to use hypoxia as a selective target. Here, we show methods and protocols using the nonpathogenic obligate anaerobic Bifidobacterium longum as a drug-delivery system (DDS) to target anaerobic tumor tissue.
MeSH term(s)	Animals ; Bifidobacterium/genetics ; Bifidobacterium/metabolism ; Disease Models, Animal ; Drug Delivery Systems ; Genetic Engineering ; Humans ; Hypoxia/metabolism ; Immunohistochemistry ; Male ; Mice ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Oxygen Consumption ; Rats ; Transplantation, Isogeneic ; Xenograft Model Antitumor Assays
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-3515-4_5
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Article ; Online: In situ delivery and production system of trastuzumab scFv with Bifidobacterium.

Kikuchi, Takeshi / Shimizu, Hitomi / Akiyama, Yasuto / Taniguchi, Shun'ichiro

Biochemical and biophysical research communications

2017 Volume 493, Issue 1, Page(s) 306–312

Abstract: A monoclonal antibody targeting human epidermal growth factor receptor-2 (HER2), trastuzumab has become a standard treatment for HER2-positive breast cancer. Recent advancements in antibody engineering have enabled the efficient generation of the ... ...

Abstract	A monoclonal antibody targeting human epidermal growth factor receptor-2 (HER2), trastuzumab has become a standard treatment for HER2-positive breast cancer. Recent advancements in antibody engineering have enabled the efficient generation of the trastuzumab single-chain variable fragment (scFv). In this study, we genetically engineered Bifidobacterium, a bacterial strain shown to accumulate safely and selectively in hypoxic tumor sites by intravenous (iv) injection, to express and secrete the trastuzumab scFv. The recombinant scFv bound to cell surface HER2 and inhibited in vitro growth of HER2-positive human cancer cells. Moreover, iv-injected recombinant bacteria specifically localized and secreted trastuzumab scFv in xenografted human HER2-positive tumors and consequently inhibited tumor growth. The development and results of this novel in situ delivery and production system for trastuzumab scFv with Bifidobacterium represents a promising avenue for future application in cancer treatment.
MeSH term(s)	Bifidobacterium/physiology ; Breast Neoplasms/microbiology ; Breast Neoplasms/pathology ; Breast Neoplasms/therapy ; Cell Line, Tumor ; Cell Survival/drug effects ; Humans ; Immunoglobulin Variable Region/administration & dosage ; Receptor, ErbB-2/metabolism ; Single-Chain Antibodies/administration & dosage ; Trastuzumab/administration & dosage ; Treatment Outcome
Chemical Substances	Immunoglobulin Variable Region ; Single-Chain Antibodies ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; Trastuzumab (P188ANX8CK)
Language	English
Publishing date	2017-11-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2017.09.026
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Article ; Online: Endothelial Dysfunction Accelerates Impairment of Mitochondrial Function in Ageing Kidneys via Inflammasome Activation.

Wada, Yoshihisa / Umeno, Reina / Nagasu, Hajime / Kondo, Megumi / Tokuyama, Atsuyuki / Kadoya, Hiroyuki / Kidokoro, Kengo / Taniguchi, Shun'ichiro / Takahashi, Masafumi / Sasaki, Tamaki / Kashihara, Naoki

International journal of molecular sciences

2021 Volume 22, Issue 17

Abstract: Chronic kidney disease is a common problem in the elderly and is associated with increased mortality. We have reported on the role of nitric oxide, which is generated from endothelial nitric oxide synthase (eNOS), in the progression of aged kidneys. To ... ...

Abstract	Chronic kidney disease is a common problem in the elderly and is associated with increased mortality. We have reported on the role of nitric oxide, which is generated from endothelial nitric oxide synthase (eNOS), in the progression of aged kidneys. To elucidate the role of endothelial dysfunction and the lack of an eNOS-NO pathway in ageing kidneys, we conducted experiments using eNOS and ASC-deficient mice. C57B/6 J mice (wild type (WT)),
MeSH term(s)	Aging ; Animals ; Endothelium/enzymology ; Endothelium/metabolism ; Endothelium/physiopathology ; Inflammasomes ; Kidney/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Mitochondria/metabolism ; Mitochondria/physiology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Vascular Diseases/physiopathology
Chemical Substances	Inflammasomes ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
Language	English
Publishing date	2021-08-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22179269
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Article: Suppression of cancer phenotypes through a multifunctional actin-binding protein, calponin, that attacks cancer cells and simultaneously protects the host from invasion.

Taniguchi, Shun'ichiro

Cancer science

2005 Volume 96, Issue 11, Page(s) 738–746

Abstract: Quantitative and/or qualitative alteration of actin cytoskeletal molecules, involved in the regulation of cellular dynamic functions, should be intimately related with cancer phenotypes. Based on several lines of experimental evidence from our group, and ...

Abstract	Quantitative and/or qualitative alteration of actin cytoskeletal molecules, involved in the regulation of cellular dynamic functions, should be intimately related with cancer phenotypes. Based on several lines of experimental evidence from our group, and others, this report proposes a strategy to simultaneously attack cancer cells and protect the host from cancer invasion, with one molecule. Calponin h1, an actin-stabilizing protein that is also intimately related to signal transduction, is very often suppressed in vascular smooth muscle cells of malignant human tumors and in mesothelial cells by coexisting cancer cells. We generated mice deficient for calponin h1, exhibiting fragility in blood vessels and peritoneal membranes. Hematogenous cancer metastasis occurred more easily in the calponin h1-deficient mice than in wild-type mice, and the peritoneal dissemination was extremely enhanced. The fragility was rescued by the exogenous introduction of the calponin h1 gene into mesothelial cells of the peritoneum. Furthermore, calponin h1 gene transfer into several transformed cell lines resulted in a suppression of malignancy. The peritoneal dissemination of intraperitoneally-injected B16-F10 cells was suppressed by the calponin h1 gene, given to target both cancer cells and the mesothelial cells of the host. The multifunctional nature of the molecule, as a machinery player of cytoskeleton and mediator of signal transduction, probably resulted in a favorable recipient-discriminating effect on cancerous and normal cells. Thus, we believe that if we use adequate multifunctional molecules for therapy, it is possible to simultaneously suppress cancer phenotypes and protect normal cells from the attack of cancer cells.
MeSH term(s)	Animals ; CARD Signaling Adaptor Proteins ; Calcium-Binding Proteins/biosynthesis ; Calcium-Binding Proteins/genetics ; Calcium-Binding Proteins/physiology ; Cell Transformation, Neoplastic ; Chemoprevention ; Cytoskeletal Proteins/physiology ; Down-Regulation ; Gene Transfer Techniques ; Humans ; Mice ; Mice, Knockout ; Microfilament Proteins ; Neoplasm Invasiveness/physiopathology ; Neoplasm Invasiveness/prevention & control ; Neoplasm Metastasis ; Neoplasms, Experimental ; Neovascularization, Pathologic ; Phenotype ; Signal Transduction ; Calponins
Chemical Substances	CARD Signaling Adaptor Proteins ; Calcium-Binding Proteins ; Cytoskeletal Proteins ; Microfilament Proteins ; PYCARD protein, human
Language	English
Publishing date	2005-11-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2111204-6
ISSN	1347-9032
ISSN	1347-9032
DOI	10.1111/j.1349-7006.2005.00118.x
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Article ; Online: Cutting Edge: G Protein Subunit β 1 Negatively Regulates NLRP3 Inflammasome Activation.

Murakami, Tomohiko / Ruengsinpinya, Lerdluck / Nakamura, Eriko / Takahata, Yoshifumi / Hata, Kenji / Okae, Hiroaki / Taniguchi, Shun'ichiro / Takahashi, Masafumi / Nishimura, Riko

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 202, Issue 7, Page(s) 1942–1947

Abstract: The NLRP3 inflammasome has important roles in the pathogenesis of various inflammatory diseases. However, the regulatory mechanisms of the NLRP3 inflammasome are not fully understood. In this study, we attempted to identify molecules that interact with ... ...

Abstract	The NLRP3 inflammasome has important roles in the pathogenesis of various inflammatory diseases. However, the regulatory mechanisms of the NLRP3 inflammasome are not fully understood. In this study, we attempted to identify molecules that interact with NLRP3 upon its activation. We identified G protein subunit β 1 (GNB1), a downstream molecule of G protein-coupled receptors (GPCRs), which regulates the NLRP3 inflammasome activation. GNB1 was physically associated with NLRP3 via the pyrin domain of NLRP3. Activation of the NLRP3 inflammasome was enhanced in GNB1-knockdown or GNB1-deficient murine macrophages, although a lack of GNB1 did not affect activation of the AIM2 inflammasome. ASC oligomerization induced by NLRP3 was enhanced by GNB1 deficiency. Conversely, NLRP3-dependent ASC oligomerization was inhibited by the overexpression of GNB1. This study indicates that GNB1 negatively regulates NLRP3 inflammasome activation by suppressing NLRP3-dependent ASC oligomerization, and it provides a regulatory mechanism of the NLRP3 inflammasome.
MeSH term(s)	Animals ; GTP-Binding Protein beta Subunits/immunology ; Inflammasomes/immunology ; Inflammation/immunology ; Macrophages/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; NLR Family, Pyrin Domain-Containing 3 Protein/immunology
Chemical Substances	GTP-Binding Protein beta Subunits ; Gnb1 protein, mouse ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
Language	English
Publishing date	2019-02-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1801388
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Article ; Online: Inflammasome and Fas-Mediated IL-1β Contributes to Th17/Th1 Cell Induction in Pathogenic Bacterial Infection In Vivo.

Uchiyama, Ryosuke / Yonehara, Shin / Taniguchi, Shun'ichiro / Ishido, Satoshi / Ishii, Ken J / Tsutsui, Hiroko

Journal of immunology (Baltimore, Md. : 1950)

2017 Volume 199, Issue 3, Page(s) 1122–1130

Abstract: ... ...

Abstract	CD4
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/deficiency ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; CARD Signaling Adaptor Proteins ; Cell Differentiation ; Inflammasomes/immunology ; Interleukin-1beta/administration & dosage ; Interleukin-1beta/immunology ; Listeria monocytogenes/immunology ; Listeria monocytogenes/pathogenicity ; Listeriosis/immunology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nuclear Receptor Subfamily 1, Group F, Member 3/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Receptors, Interleukin-1 Type I/genetics ; Receptors, Interleukin-1 Type I/immunology ; Spleen/immunology ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Th1 Cells/immunology ; Th17 Cells/immunology ; fas Receptor/deficiency ; fas Receptor/genetics ; fas Receptor/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; CARD Signaling Adaptor Proteins ; Fas protein, mouse ; IL1R1 protein, mouse ; Inflammasomes ; Interleukin-1beta ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Pycard protein, mouse ; Receptors, Interleukin-1 Type I ; T-Box Domain Proteins ; T-box transcription factor TBX21 ; fas Receptor
Language	English
Publishing date	2017-08-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1601373
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