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Bacille Calmette Guérin (BCG) can induce Kawasaki disease-like features in programmed death-1 (PD-1) gene knockout mice

Authors
 J. Chun  ;  B. Jeon  ;  D. Kang  ;  D. Kim 
Citation
 CLINICAL AND EXPERIMENTAL RHEUMATOLOGY, Vol.29(4) : 743-750, 2011 
Journal Title
CLINICAL AND EXPERIMENTAL RHEUMATOLOGY
ISSN
 0392-856X 
Issue Date
2011
MeSH
Animals ; Antigens, Surface/genetics ; Apoptosis Regulatory Proteins/deficiency* ; Apoptosis Regulatory Proteins/genetics ; Bacterial Proteins/immunology ; Biliary Tract/blood supply ; Chaperonin 60/immunology ; Coronary Vessels/immunology ; Coronary Vessels/pathology ; Disease Models, Animal ; Female ; Hepatic Artery/immunology ; Hepatic Artery/pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Mucocutaneous Lymph Node Syndrome/etiology* ; Mucocutaneous Lymph Node Syndrome/genetics ; Mucocutaneous Lymph Node Syndrome/immunology ; Mucocutaneous Lymph Node Syndrome/microbiology ; Mucocutaneous Lymph Node Syndrome/pathology ; Mycobacterium bovis/immunology* ; Programmed Cell Death 1 Receptor ; Renal Artery/immunology ; Renal Artery/pathology ; Spleen/immunology ; Staphylococcus aureus/immunology ; T-Lymphocytes/immunology
Keywords
coronary arterial disease ; gene ; mucocutaneous lymph node syndrome ; programmed death-1 ; inflammation
Abstract
OBJECTIVES: Various genetic variants of inhibitory immune signals have been suspected as feasible causes of Kawasaki disease (KD). We investigated the associative role of programmed death-1 (PD-1) gene in the pathogenesis of KD by injecting bacilli Calmette Guérin (BCG) to PD-1 gene knockout (PD-1KO) mice.

METHODS: In order to induce KD-like clinical manifestations in young PD-1KO mice, intradermal injection of the bacilli Calmette Guérin (BCG) was performed twice on the abdominal skin with a 4-week interval. For defining the role of BCG, heat shock protein (HSP) 65 was challenged. In addition, Staphylococcus aureus was adopted as a microorganism that does not contain HSP65 structure. One month after the second injection, heart, liver, and kidneys were removed and examined.

RESULTS: PD-1KO mice showed KD-like features including prolonged fever for more than 5 days, erythematous swelling on soles, tail skin desquamation, and gallbladder (GB) hydrops. Inflammatory cell aggregation and intimal proliferation in at least more than one coronary artery was found in all PD-1KO mice whereas scanty coronary lesion was found in wild type (WT) mice. When the PD-1KO mice were injected twice with HSP65, coronary arterial lesions similar to those seen after BCG injection were observed. Inflammatory reactions in other organs including hepatic arteries, renal arteries, and biliary arteries were also observed in PD-1KO mice.

CONCLUSIONS: Our data suggest that PD-1 gene may be one of the genetic predispositions of KD and antigens containing HSP65 structure could be a triggering factor of KD by our animal model of KD.
Full Text
http://www.clinexprheumatol.org/pubmed/find-pii.asp?pii=21906434
Appears in Collections:
1. College of Medicine (의과대학) > Research Institute (부설연구소) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pediatrics (소아과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Dong Soo(김동수)
Jeon, Bo Young(전보영)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/93711
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