Experimental Chemotherapy in Paracoccidioidomycosis Using Ruthenium NO Donor
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  • 作者：1. Department of Pathology Science ; CCB ; State University of Londrina-UEL ; Londrina ; PR ; Brazil2. Institute of Physics of S?o Carlos ; University of S?o Paulo-USP ; S?o Paulo ; Brazil3. Department of Pharmacology ; Faculty Medicine of Ribeir?o Preto-USP ; Ribeir?o Preto ; Brazil4. Department of Organic and Inorganic Chemistry ; Federal University of Ceará ; Fortaleza ; Brazil5. Universidade Estadual de Londrina-UEL-Rodovia Celso Garcia Cid ; Campus Universitário ; Cx. Postal 6001 ; Londrina ; PR 86051-990 ; Brazil
  • 关键词：Ruthenium nitrosyl – NO donors – Nitric oxide – Paracoccidioidomycosis
  • 刊名：Mycopathologia
  • 出版年：2011
  • 出版时间：August 2011
  • 年：2011
  • 卷：172
  • 期：2
  • 页码：95-107
  • 全文大小：818.7 KB
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  • 作者单位：http://www.springerlink.com/content/r11n277271p515v8/
  • 刊物类别：Biomedical and Life Sciences
  • 刊物主题：Life Sciences
    Microbiology
    Medical Microbiology
    Plant Sciences
    Microbial Ecology
  • 出版者：Springer Netherlands
  • ISSN：1573-0832
文摘
Paracoccidioidomycosis (PCM) is a granulomatous disease caused by a dimorphic fungus, Paracoccidioides brasiliensis (Pb). To determine the influence of nitric oxide (NO) on this disease, we tested cis-[Ru(bpy)2(NO)SO3](PF6), ruthenium nitrosyl, which releases NO when activated by biological reducing agents, in BALB/c mice infected intravenously with Pb 18 isolate. In a previous study by our group, the fungicidal activity of ruthenium nitrosyl was evaluated in a mouse model of acute PCM, by measuring the immune cellular response (DTH), histopathological characteristics of the granulomatous lesions (and numbers), cytokines, and NO production. We found that cis-[Ru(bpy)2(NO)SO3](PF6)-treated mice were more resistant to infection, since they exhibited higher survival when compared with the control group. Furthermore, we observed a decreased influx of inflammatory cells in the lung and liver tissue of treated mice, possibly because of a minor reduction in fungal cell numbers. Moreover, an increased production of IL-10 and a decrease in TNF-α levels were detected in lung tissues of infected mice treated with cis-[Ru(bpy)2(NO)SO3](PF6). Immunohistochemistry showed that there was no difference in the number of VEGF- expressing cells. The animals treated with cis-[Ru(bpy)2(NO)SO3](PF6) showed high NO levels at 40 days after infection. These results show that NO is effectively involved in the mechanism that regulates the immune response in lung of Pb-infected mice. These data suggest that NO is a resistance factor during paracoccidioidomycosis by controlling fungal proliferation, influencing cytokine production, and consequently moderating the development of a strong inflammatory response.

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