Prevention of late lumen loss after coronary angioplasty by photodynamic therapy: Role of activated neutrophils

Sluiter, Wim J.; Vree, W. J. A. De; Pietersma, Anneke; Koster, J.F.

doi:10.1007/978-1-4613-1275-8_30

Cited by 7 publications

(10 citation statements)

References 35 publications

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“…Sluiter et al 85 first observed that neutrophils adhere to the microvascular wall after PDT in vivo, but PDT did not stimulate the expression of P-selectin (one of the principal adhesion molecules that bind leukocytes) by endothelial cells (ECs). The ECs retracted after PDT, which enabled neutrophils to adhere to the subendothelial matrix by their β2-integrin adhesion receptors, and this could be blocked by anti-β2-integrin antibodies86.…”

Section: Neutrophil Recruitment and The Production Of Il6mentioning

confidence: 99%

“…The depletion of neutrophils did not significantly change the high cure rates of that regimen, but abolished curability in the maximally inflammatory regimen. These data indicate that tumour cure can be mediated by maximizing the photochemical action of PDT, but the importance of causing inflammation and neutrophil infiltration is less clear.Sluiter et al 85 first observed that neutrophils adhere to the microvascular wall after PDT in vivo, but PDT did not stimulate the expression of P-selectin (one of the principal adhesion molecules that bind leukocytes) by endothelial cells (ECs). The ECs retracted after PDT, which enabled neutrophils to adhere to the subendothelial matrix by their β2-integrin adhesion receptors, and this could be blocked by anti-β2-integrin antibodies86.…”

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Photodynamic therapy and anti-tumour immunity

2006

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Photodynamic therapy (PDT) uses non-toxic photosensitizers and harmless visible light in combination with oxygen to produce cytotoxic reactive oxygen species that kill malignant cells by apoptosis and/or necrosis, shut down the tumour microvasculature and stimulate the host immune system. In contrast to surgery, radiotherapy and chemotherapy that are mostly immunosuppressive, PDT causes acute inflammation, expression of heat-shock proteins, invasion and infiltration of the tumour by leukocytes, and might increase the presentation of tumour-derived antigens to T cells.The principle of photodynamic therapy (PDT) was first proposed over 100 years ago 1 . A recent review in Nature Reviews Cancer by Rakesh Jain and colleagues described some of the historical milestones in the development of PDT as a cancer treatment2. Many of the photosensitizers (PSs) that have been studied since PDT was first proposed are based on a porphyrin-like nucleus 3 . PSs function as catalysts when they absorb visible light and then convert molecular oxygen to a range of highly reactive oxygen species (ROS). The ROS that are produced during PDT have been shown to destroy tumours by multifactorial mechanisms4 , 5 (FIG. 1). PDT has a direct affect on cancer cells, producing cell death by necrosis and/or apoptosis 6 . PDT also has an affect on the tumour vasculature, whereby illumination and ROS production causes the shutdown of vessels and subsequently deprives the tumour of oxygen and nutrients 7,8 . Finally, PDT also has a significant effect on the immune system 9-11 , which can be either immunostimulatory or immunosuppressive.Most of the commonly used cancer therapies are immunosuppressive. Chemotherapy and ionizing radiation delivered at doses sufficient to destroy tumours are known to be toxic to the bone marrow, which is the source of all cells of the immune system, and neutropaenia and other forms of myelosuppression are often the dose-limiting toxicity of these therapies. However, it should be noted that low doses of either ionizing radiation12 , 13 or chemotherapy14 can have immunostimulatory effects, including the induction of heat-shock © 2006 Nature Publishing Group Correspondence to M.R.H. Hamblin@helix.mgh.harvard.edu. Competing interests statementThe authors declare no competing financial interests. DATABASES NIH Public Access Author ManuscriptNat Rev Cancer. Author manuscript; available in PMC 2010 September 6. Published in final edited form as:Nat Rev Cancer. 2006 July ; 6(7): 535-545. doi:10.1038/nrc1894. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript proteins 15 . Less well known is the fact that major surgery can also have an immunosuppressive effect that leads to a significant diminution of lymphocyte and natural killer (NK) cell function 16 . The ideal cancer therapy would not only destroy the primary tumour, but at the same time trigger the immune system to recognize, track down and destroy any remaining tumour cells, be they at or near the site of the primary tumour or distant microm...

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Section: Neutrophil Recruitment and The Production Of Il6mentioning

confidence: 99%

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confidence: 99%

Photodynamic therapy and anti-tumour immunity

2006

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“…E-selectin. Other studies have shown that PDT-induced adherence of neutrophils to endothelial cells in vitro (de Vree et al, 1996b) and in vivo (Dellian et al, 1995;Adili et al, 1996;Sluiter et al, 1996;Rousset et al, 1999) also involved b 2 -integrins (LFA-1) (Sluiter et al, 1996;de Vree et al, 1996b). Blocking E-selectin and MIP-2 action through the use of neutralising antibodies, administered immediately after completion of PDT treatment, led to a significant reduction in neutrophil accumulation to almost baseline levels by 6 h post-treatment (PDT+anti-MIP-2 vs PDT+rat IgG: Po0.0024; PDT+anti-E-selectin vs PDT+rat IgG: Po0.04) ( Figure 5B).…”

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confidence: 98%

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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“…Interestingly, it has been shown that photosensitization with Photofrin ® caused polymorphonuclear leukocytes to adhere to the wall of normal vessel (7) but not to those of tumor capillaries (8). Despite the adherence of neutrophils to the microvascular wall after PDT in vivo, the expression of P-selectin (one of the main adhesion molecules that bind leukocytes) by endothelial cells (EC) was not stimulated (9) but the expression of the adhesion molecule Figure 3). The expression levels of the adhesion molecules ICAM-1 and vascular cell adhesion molecule 1 were down-regulated in EC after PDT (12).…”

Section: Adhesion Moleculesmentioning

confidence: 99%

Effect of photodynamic therapy on the extracellular matrix and associated components

Pazos

Nader

2007

Braz J Med Biol Res

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In many countries, photodynamic therapy (PDT) has been recognized as a standard treatment for malignant conditions (for example, esophageal and lung cancers) and non-malignant ones such as age-related macular degeneration and actinic keratoses. The administration of a non-toxic photosensitizer, its selective retention in highly proliferating cells and the later activation of this molecule by light to form reactive oxygen species that cause cell death is the principle of PDT. Three important mechanisms are responsible for the PDT effectiveness: a) direct tumor cell kill; b) damage of the tumor vasculature; c) post-treatment immunological response associated with the leukocyte stimulation and release of many inflammatory mediators like cytokines, growth factors, components of the complement system, acute phase proteins, and other immunoregulators. Due to the potential applications of this therapy, many studies have been reported regarding the effect of the treatment on cell survival/death, cell proliferation, matrix assembly, proteases and inhibitors, among others. Studies have demonstrated that PDT alters the extracellular matrix profoundly. For example, PDT induces collagen matrix changes, including cross-linking. The extracellular matrix is vital for tissue organization in multicellular organisms. In cooperation with growth factors and cytokines, it provides cells with key signals in a variety of physiological and pathological processes, for example, adhesion/migration and cell proliferation/differentiation/death. Thus, the focus of the present paper is related to the effects of PDT observed on the extracellular matrix and on the molecules associated with it, such as, adhesion molecules, matrix metalloproteinases, growth factors, and immunological mediators.

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Prevention of late lumen loss after coronary angioplasty by photodynamic therapy: Role of activated neutrophils

Cited by 7 publications

References 35 publications

Photodynamic therapy and anti-tumour immunity

Photodynamic therapy and anti-tumour immunity

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

Effect of photodynamic therapy on the extracellular matrix and associated components

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