 8/10 Excellent --- eutils.ncbi.nlm.nih.gov http://eutils.ncbi.nlm.nih.gov/entrez/eutils/erss.cgi?rss_guid=0knUDwkUyt5fupC2d
| NCBI: db=PubMed; Term=macrophages vegf ... |
Wednesday, August 06, 2008 --- 14 days ago http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?tmpl=NoSidebarfile&db=PubMed&cmd=R
| Related Articles Seoul virus enhances regulatory and reduces proinflammatory responses in male Norway rats. J Med Virol. 2008 Jul;80(7):1308-18 Authors: Easterbrook JD, Klein SL Zoonotic pathogens, including hantaviruses, are maintained in the environment by causing persistent infection in the absence of disease in their reservoir hosts. Spillover of hantaviruses to humans can cause severe disease that is mediated by excessive proinflammatory responses. The mechanisms mediating hantaviral persistence in rodent reservoirs remain largely unknown. Male Norway rats were inoculated with their species-specific hantavirus, Seoul virus (SEOV), and viral RNA, cytokine, and chemokine responses were evaluated in spleen and lung tissue. More viral RNA was detectable in the lungs than spleen, with copies of SEOV peaking 15-30 days post-inoculation (p.i.) and persisting for 60 days p.i. In the lungs, the expression and production of proinflammatory mediators (i.e., IL-1beta, IL-6, TNF-alpha, IFN-gamma, CCL5, CCL2, CX3CL1, CXCL10, VCAM, VEGF, and NOS2) remained at or below baseline throughout SEOV infection; whereas, regulatory factors, including TGF-beta and FoxP3 were elevated. Conversely, in the spleen, proinflammatory responses were induced while regulatory responses remained unchanged during infection. To determine whether reduced proinflammatory responses mediate hantavirus persistence in the lungs, male rats were administered rIL-1beta or vehic ... |
|
|
Anytime
