Local hyperthermia could induce antiviral activity by endogenous interferon-dependent pathway in condyloma acuminata
Autor: | Yuxiao Hong, Xing-Hua Gao, Li Zhang, Xiaoqin Wang, Hong-Duo Chen, Li-Li Zhu, Xiaodong Li, Uwesu Omari Mchepange, Huachen Wei, Ruiqun Qi |
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Rok vydání: | 2010 |
Předmět: |
Male
Hyperthermia Hot Temperature medicine.medical_treatment Gene Expression Endogeny Biology Virus Replication Antiviral Agents Interferon-gamma eIF-2 Kinase Interferon Virology 2' 5'-Oligoadenylate Synthetase medicine Humans Protein kinase A Skin Pharmacology Human papillomavirus 11 Kinase Interferon-alpha Hyperthermia Induced Interferon-beta Protein-Tyrosine Kinases Human papillomavirus 6 medicine.disease DNA-Binding Proteins STAT Transcription Factors Cytokine Condylomata Acuminata Tyrosine kinase 2 Immunology Cancer research Female Interferons Signal transduction Signal Transduction medicine.drug |
Zdroj: | Antiviral Research. 88:187-192 |
ISSN: | 0166-3542 |
Popis: | Local hyperthermia has been successfully used in the treatment of viral warts by mechanisms that have largely remained unclear. Using an organotypic culture system, we found that hyperthermia at 42 °C and 45 °C could induce a significant increase in the transcriptional expression of interferon (IFN)-α, IFN-β and IFN-γ, in a temperature-dependent manner in condyloma acuminata (CA), but not in normal skin. Accordingly, local hyperthermia could enhance the expression of 2′-5′ oligoadenylate synthase and double-stranded RNA (dsRNA)-dependent protein kinase, two antiviral enzymes downstream of the IFN-dependant pathway. Hyperthermia led to an increase in IFN-α/β receptor transcripts, and an increase in the levels in phospho-Stat1 and phospho-Stat2 in CA, though it had no influence on the levels of Jak1, Tyk2, Stat1 and Stat2 transcriptional expression. Local hyperthermia was proved effective in treating human papillomavirus-infected skin. These results suggested that hyperthermia took effect partly by inducing the expression of local endogenous IFN and partly by subsequent IFN-induced antiviral activity via Jak–STATs signalling pathway in CA. |
Databáze: | OpenAIRE |
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