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Thalidomide upregulates macrophage inflammatory protein-1alpha in a herpes simplex virus-induced Behçet's disease-like animal model.

Authors
Lee, ES; Kim, YA; Kwon, HJ; Bang, D; Lee, S; Sohn, S
Citation
Archives of dermatological research, 296(4):175-181, 2004
Journal Title
Archives of dermatological research
ISSN
0340-36961432-069X
Abstract
The mechanism of action of thalidomide in the treatment of patients with Behçet's disease (BD) is poorly understood. There is some evidence to suggest that certain immunological abnormalities are associated with the pathogenesis of BD. A BD-like mouse model induced by herpes simplex virus (HSV) inoculation shows similar immunological abnormalities. In this study, thalidomide was administered in order to understand the mechanism for the improvement in symptoms in BD-like mice. Eight out of ten thalidomide-treated mice showed improvement but none of ten placebo-treated mice (P < 0.005). The improvements were seen in mucocutaneous symptoms. The mice were sacrificed on the 6th day, and the spleens subjected to RT-PCR, FACS, Western blot and immunohistochemical analysis. IL-2, IL-4, IL-6, IL-10, IFN-gamma, TNFalpha, TGFbeta, MCP-1, RANTES, perforin, IP-10, FasL, FasR and MIP-lalpha were determined. Among these, TNFalpha, MIP-1alpha, perforin and Fas were influenced by thalidomide treatment. These results suggest that thalidomide can attenuate HSV-induced BD-like symptoms in mice through the downregulation of TNFalpha (P < 0.005) and the upregulation of MIP-1alpha (P < 0.005), perforin (P < 0.05) and FasR (P < 0.1).
MeSH terms
AnimalsAntigens, CD95/geneticsApoptosis/drug effectsBehcet Syndrome/*metabolism/physiopathology/*virologyCells, CulturedChemokine CCL3Chemokine CCL4Disease Models, AnimalDown-RegulationHerpes Simplex/*complicationsImmunosuppressive Agents/*pharmacologyMacrophage Inflammatory Proteins/genetics/*metabolismMaleMembrane Glycoproteins/geneticsMiceMice, Inbred ICRPerforinPore Forming Cytotoxic ProteinsRNA, Messenger/metabolismSpleen/drug effects/metabolism/pathology/physiopathologyThalidomide/*pharmacologyTumor Necrosis Factor-alpha/geneticsUp-Regulation
DOI
10.1007/s00403-004-0498-8
PMID
15290170
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Dermatology
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
AJOU Authors
이, 은소손, 성향
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