| Interleukin-1α is the major alarmin of lung epithelial cells released during photodynamic therapy to induce inflammatory mediators in fibroblasts. | |
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MedLine Citation:
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PMID: 22996613 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Photodynamic therapy (PDT) causes tissue damage that initiates a local inflammatory response. Post-PDT reactions are considered to assist in mobilising the immune system thereby affecting tumour recurrence. The initiating process of the PDT-dependent tissue reaction remains to be determined. METHODS: Primary cultures of human lung cells were established. The photoreaction mediated by pyropheophorbide-a, at specific subcellular sites and levels resulting in the release of alarmins by epithelial cells (Eps), was defined by immunoblot analyses and expression profiling. The activity of Ep-derived factors to stimulate expression of proinflammatory mediators, including IL-6, and to enhance neutrophil binding by fibroblasts (Fbs) was determined by functional bioassays. RESULTS: Epithelial cells release IL-1β as the primary Fb-stimulatory activity under basal conditions. Intracellular IL-1α, externalised following photoreaction, accounts for most of the PDT-mediated Fb activation. Expression of IL-1 is subject to increase or loss during oncogenic transformation resulting in altered alarmin functions mobilisable by PDT. Photoreaction by a cell surface-bound photosensitiser (PS) is 10-fold more effective than PSs localised to mitochondria or lysosomes. High-dose intracellular, but not cell surface, photoreaction inactivates IL-1 and reduces Fb stimulation. CONCLUSION: These in vitro data suggest that the subcellular site and intensity of photoreaction influence the magnitude of the stromal cell response to the local damage and, in part, support the relationship of PDT dose and level of post-PDT inflammatory response observed in vivo. |
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Authors:
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E C Tracy; M J Bowman; B W Henderson; H Baumann |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-09-20 |
Journal Detail:
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Title: British journal of cancer Volume: 107 ISSN: 1532-1827 ISO Abbreviation: Br. J. Cancer Publication Date: 2012 Oct |
Date Detail:
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Created Date: 2012-10-24 Completed Date: 2013-03-21 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0370635 Medline TA: Br J Cancer Country: England |
Other Details:
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Languages: eng Pagination: 1534-46 Citation Subset: IM |
Affiliation:
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Departments of Molecular and Cellular Biology, Roswell Park Cancer Institute, Elm and Carlton Streets, Buffalo, NY 14263, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Epithelial Cells / drug effects, metabolism Fibroblasts / drug effects, metabolism Humans Inflammation Mediators / metabolism* Interleukin-1alpha / metabolism* Lung / cytology, drug effects*, metabolism* Photochemotherapy / methods* Rats |
| Grant Support | |
ID/Acronym/Agency:
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P01CA55791/CA/NCI NIH HHS; P30CA16056/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Inflammation Mediators; 0/Interleukin-1alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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