Enhancing Effect of an Inhibitor of Nitric Oxide Synthesis on Bacillus Calmette‐Guérin‐induced Macrophage Cytotoxicity against Murine Bladder Cancer Cell Line MBT‐2 <i>in vitro</i>

Yamada, Hiroshi; Matsumoto, Sohkichi; Matsumoto, Tetsuro; Yamada, Takeshi; Yamashita, Uki

doi:10.1111/j.1349-7006.2000.tb00978.x

Cited by 19 publications

(24 citation statements)

References 41 publications

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“…In a previous paper we have reported that BCG-induced macrophage-mediated cytotoxicity was regulated by soluble factors such as IFN-g and TNF-a [20]. We also found that IFN-g and TNF-a production by PEC were down-regulated by PGE 2 and up-regulated by COX inhibitors (Fig.…”

Section: Discussionsupporting

confidence: 60%

Prostaglandin E2 down-regulates viable Bacille Calmette–Guérin-induced macrophage cytotoxicity against murine bladder cancer cell MBT-2in vitro

Yamada

Kuroda

Matsumoto

et al. 2002

Clinical and Experimental Immunology

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SUMMARY The regulatory effect of prostaglandin (PG) E2 and a cyclooxygenase (COX) inhibitor on Bacille Calmette–Guérin (BCG)‐induced macrophage cytotoxicity in a bladder cancer cell, MBT‐2, was studied in vitro. BCG stimulated thioglycollate‐elicited murine peritoneal exudate cells (PEC) to induce cytotoxic activity and to produce cytokines such as interferon (IFN)‐γ, tumour necrosis factor (TNF)‐α and PGE2. NS398, a specific COX‐2 inhibitor, and indomethacin (IM), a COX‐1 and COX‐2 inhibitor, enhanced viable BCG‐induced cytotoxic activity and IFN‐γ and TNF‐α production of PEC. However, NS398 and IM did not enhance these activities induced by killed BCG. Enhanced cytotoxicity was mediated by increased amounts of IFN‐γ and TNF‐α. Exogenous PGE2 reduced cytotoxic activity and IFN‐γ and TNF‐α production of PEC. These results suggest that PGE2 produced by BCG‐activated macrophages has a negative regulatory effect on the cytotoxic activity of macrophages. Accordingly, a PG synthesis inhibitor may be a useful agent to enhance BCG‐induced antitumour activity of macrophages.

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Section: Discussionsupporting

confidence: 60%

Prostaglandin E2 down-regulates viable Bacille Calmette–Guérin-induced macrophage cytotoxicity against murine bladder cancer cell MBT-2in vitro

Yamada

Kuroda

Matsumoto

et al. 2002

Clinical and Experimental Immunology

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“…We previously demonstrated that macrophages exhibited cytotoxicity against MBT‐2 cells (a mouse bladder cancer line of C3H origin) in vitro upon BCG activation [46,47]. In these studies, PECs were used as a conventional source for macrophages.…”

Section: Discussionmentioning

confidence: 99%

RecombinantMycobacterium bovisbacillus Calmette-Guérin (BCG) expressing mouse IL-18 augments Th1 immunity and macrophage cytotoxicity

Luo

Yamada

Chen

et al. 2004

Clinical and Experimental Immunology

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SUMMARY has been demonstrated to synergize with BCG for induction of a T-helper-type 1 (Th1) immune response. Since successful treatment of superficial bladder cancer with BCG requires proper induction of Th1 immunity, we have developed a recombinant (r) BCG strain that functionally secretes mouse (m) IL-18. This rBCG-mIL-18 strain significantly increased production of the major Th1 cytokine IFN-g in splenocyte cultures, at levels comparable to that elicited by control BCG plus exogenous rIL-18. IFN-g production by splenocytes was eliminated by addition of neutralizing anti-IL-18 antibody. Endogenous IL-12 played a favourable role whereas IL-10 played an adverse role in rBCGmIL-18-induced IFN-g production. Enhanced host antimycobacterial immunity was observed in mice infected with rBCG-mIL-18 which showed less splenic enlargement and reduced bacterial load compared to control mice infected with BCG. Further, splenocytes from rBCG-mIL-18-infected mice, in response to BCG antigen, displayed increased production of IFN-g and GMCSF, decreased production of IL-10, elevated cellular proliferation and higher differentiation of IFN-g -secreting cells. rBCG-mIL-18 also enhanced BCG-induced macrophage cytotoxicity against bladder cancer MBT-2 cells in a dosedependent manner. Neutralizing all endogenous macrophage-derived cytokines tested (IL-12, IL-18 and TNF-a ) as well as IFN-g severely diminished the rBCG-mIL-18-induced macrophage cytolytic activity, indicating a critical role for these cytokines in this process. Cytokine analysis for supernatants of macrophage-BCG mixture cultures manifested higher levels of IFN-g and TNF-a in rBCG-mIL-18 cultures than in control BCG cultures. Taken together, this rBCG-mIL-18 strain augments BCG's immunostimulatory property and may serve as a better agent for bladder cancer immunotherapy and antimycobacterial immunization.

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“…Injection of cytostatics to macrophages, for example silica or antimacrophage serum, in vivo, could accelerate the growth of tumor (Irie, et al, 2005). However, the Bacille Calmette Guerin or coryne bacterium parvum could restrain tumor growth and metastasis by activated macrophages (Yamada et al, 2000;Luo et al, 2004). Pathology biopsy showed that if there were macrophages around the tumor tissue, the incidence rate of the tumor metastasis was lower and the prognosis showed better also.…”

Section: Discussionmentioning

confidence: 99%

Kupffer Cells Suppress Hepatocarcinogenesis and Metastasis in Tumor Orthotopic Implanted Kunming Mice

Li¹,

Wang²,

Zhang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Enhancing Effect of an Inhibitor of Nitric Oxide Synthesis on Bacillus Calmette‐Guérin‐induced Macrophage Cytotoxicity against Murine Bladder Cancer Cell Line MBT‐2 in vitro

Cited by 19 publications

References 41 publications

Prostaglandin E2 down-regulates viable Bacille Calmette–Guérin-induced macrophage cytotoxicity against murine bladder cancer cell MBT-2in vitro

Prostaglandin E2 down-regulates viable Bacille Calmette–Guérin-induced macrophage cytotoxicity against murine bladder cancer cell MBT-2in vitro

RecombinantMycobacterium bovisbacillus Calmette-Guérin (BCG) expressing mouse IL-18 augments Th1 immunity and macrophage cytotoxicity

Kupffer Cells Suppress Hepatocarcinogenesis and Metastasis in Tumor Orthotopic Implanted Kunming Mice

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