Urinary cytokines following photodynamic therapy for bladder cancer a preliminary report

Nseyo, Unyime O.; Whalen, Raymond K.; Duncan, Matthew R.; Berman, Brian; Lundahl, Scott L.

doi:10.1016/0090-4295(90)80220-h

Cited by 73 publications

(32 citation statements)

References 10 publications

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“…In PDT employing the photosensitiser Photofrin s , the combined effects on these tissue targets result in an intense inflammatory response and tumour involution within 24 h. The inflammatory response is considered an important priming event for the development of specific antitumour immunity associated with Photofrin s PDT (Korbelik, 1996;Korbelik and Cecic, 1998;Dougherty et al, 1998). Photofrin s -PDT-induced inflammatory changes are characterised by enhanced expression of a number of proinflammatory cytokines, including interleukin (IL)-1b, tumour necrosis factor (TNF)-a and IL-6 (Evans et al, 1990;Nseyo et al, 1990;Kick et al, 1995;Gollnick et al, 1997). PDT-induced inflammation is accompanied by leucocyte infiltration into the treated tumour.…”

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confidence: 99%

Role of cytokines in photodynamic therapy-induced local and systemic inflammation

et al. 2003

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Photodynamic therapy (PDT) of tumour results in the rapid induction of an inflammatory response that is considered important for the activation of antitumour immunity, but may be detrimental if excessive. The response is characterised by the infiltration of leucocytes, predominantly neutrophils, into the treated tumour. Several preclinical studies have suggested that suppression of longterm tumour growth following PDT using Photofrin s is dependent upon the presence of neutrophils. The inflammatory pathways leading to the PDT-induced neutrophil migration into the treated tumour are unknown. In the following study, we examined, in mice, the ability of PDT using the second-generation photosensitiser 2-[1-hexyloxyethyl]-2-devinyl pyropheophorbide-a (HPPH) to induce proinflammatory cytokines and chemokines, as well as adhesion molecules, known to be involved in neutrophil migration. We also examined the role that these mediators play in PDT-induced neutrophil migration. Our studies show that HPPH-PDT induced neutrophil migration into the treated tumour, which was associated with a transient, local increase in the expression of the chemokines macrophage inflammatory protein (MIP)-2 and KC. A similar increase was detected in functional expression of adhesion molecules, that is, E-selectin and intracellular adhesion molecule (ICAM)-1, and both local and systemic expression of interleukin (IL)-6 was detected. The kinetics of neutrophil immigration mirrored those observed for the enhanced production of chemokines, IL-6 and adhesion molecules. Subsequent studies showed that PDT-induced neutrophil recruitment is dependent upon the presence of MIP-2 and E-selectin, but not on IL-6 or KC. These results demonstrate a PDT-induced inflammatory response similar to, but less severe than obtained with Photofrin s PDT. They also lay the mechanistic groundwork for further ongoing studies that attempt to optimise PDT through the modulation of the critical inflammatory mediators.

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confidence: 99%

Role of cytokines in photodynamic therapy-induced local and systemic inflammation

et al. 2003

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“…However, several studies have indicated that local PDT treatment of tumours can result in wide-spread effects including systemic neutrophilia (Cecic et al, 2001), induction of acute-phase proteins (Cecic et al, 2001;Gollnick et al, 2003), increased circulating levels of complement proteins (Cecic et al, 2006) and systemic release of pro-inflammatory cytokines (Nseyo et al, 1990;Ziolkowski et al, 1996;de Vree et al, 1997;Cecic and Korbelik, 2002;Gollnick et al, 2003;Yom et al, 2003), all of which indicate the presence of a systemic inflammatory response. Subsequent studies showed that local PDT treatment of murine tumours results in the induction of anti-tumour immunity and resistance to subsequent tumour challenge (reviewed in Canti et al, 2002;Castano et al, 2006).…”

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CD8+ T cell-mediated control of distant tumours following local photodynamic therapy is independent of CD4+ T cells and dependent on natural killer cells

et al. 2007

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Cancer survival rates decrease in the presence of disseminated disease. However, there are few therapies that are effective at eliminating the primary tumour while providing control of distant stage disease. Photodynamic therapy (PDT) is an FDA-approved modality that rapidly eliminates local tumours, resulting in cure of early disease and palliation of advanced disease. Numerous preclinical studies have shown that local PDT treatment of tumours enhances anti-tumour immunity. We hypothesised that enhancement of a systemic anti-tumour immune response might control the growth of tumours present outside the treatment field. To test this hypothesis we delivered PDT to subcutaneous (s.c.) tumours of mice bearing both s.c. and lung tumours and monitored the growth of the untreated lung tumours. Our results demonstrate that PDT of murine tumours provided durable inhibition of the growth of untreated lung tumours. The inhibition of the growth of tumours outside the treatment field was tumour-specific and dependent on the presence of CD8 þ T cells. This inhibition was accompanied by an increase in splenic anti-tumour cytolytic activity and by an increase in CD8 þ T cell infiltration into untreated tumours. Local PDT treatment led to enhanced anti-tumour immune memory that was evident 40 days after tumour treatment and was independent of CD4 þ T cells. CD8 þ T cell control of the growth of lung tumours present outside the treatment field following PDT was dependent upon the presence of natural killer (NK) cells. These results suggest that local PDT treatment of tumours lead to induction of an anti-tumour immune response capable of controlling the growth of tumours outside the treatment field and indicate that this modality has potential in the treatment of distant stage disease.

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“…Previous studies showed that cytokines could be released by the PDT-treated tumours. [1][2][3][4][5] The tumourderived cytokines may attract the migration of neutrophils and phagocytes to the tumour bed and eliminate the cell debris caused by PDT. Macrophages can be also activated to destroy the remaining tumour cells and to prevent distant metastasis.…”

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confidence: 99%

Photodynamic therapy-mediated modulation of inflammatory cytokine production by Epstein–Barr virus-infected nasopharyngeal carcinoma cells

Koon

Leung

et al. 2010

Cell Mol Immunol

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Nasopharyngeal carcinoma (NPC) is a malignant disease associated with Epstein-Barr virus (EBV) infection. This study aims to examine the effects of EBV infection on the production of proinflammatory cytokines in NPC cells after the Zn-BC-AM photodynamic therapy (PDT) treatment. Cells were treated with the photosensitiser Zn-BC-AM for 24 h before light irradiation. Quantitative ELISA was used to evaluate the production of cytokines. Under the same experimental condition, HK-1-EBV cells produced a higher basal level of IL-1a (1561 pg/ml), IL-1b (16.6 pg/ml) and IL-8 (422.9 pg/ml) than the HK-1 cells. At the light dose of 0.25-0.5 J/cm 2 , Zn-BC-AM PDT-treated HK-1-EBV cells were found to produce a higher level of IL-1a and IL-1b than the HK-1 cells. The production of IL-1b appeared to be mediated via the IL-1b-converting enzyme (ICE)-independent pathway. In contrast, the production of angiogenic IL-8 was downregulated in both HK-1 and HK-1-EBV cells after Zn-BC-AM PDT. Our results suggest that Zn-BC-AM PDT might indirectly reduce tumour growth through the modulation of cytokine production.

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Urinary cytokines following photodynamic therapy for bladder cancer a preliminary report

Cited by 73 publications

References 10 publications

Role of cytokines in photodynamic therapy-induced local and systemic inflammation

Role of cytokines in photodynamic therapy-induced local and systemic inflammation

CD8+ T cell-mediated control of distant tumours following local photodynamic therapy is independent of CD4+ T cells and dependent on natural killer cells

Photodynamic therapy-mediated modulation of inflammatory cytokine production by Epstein–Barr virus-infected nasopharyngeal carcinoma cells

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