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Published on: September 14, 2010
Human cytomegalovirus pUL135 protein affects endothelial cell function via CD2AP in Kawasaki disease
Lili Yu1, Yucui Li2, Yingying Zhang2
1Pediatric Research Institute, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Wenzhou, Zhejiang, China; Key Laboratory of Structural Malformations in Childern of Zhejiang Province, 325027, Wenzhou, Zhejiang, China; Department of Pediatrics, and Key Laboratory of Children Genitourinary Diseases of Wenzhou, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Background:
Kawasaki disease (KD) is a kind of pediatric vasculitis, whose pathogenesis has not been elucidated until now. Many scholars believe that KD is one type of infectious diseases in the susceptible groups. However, no recognized pathogens are confirmed. Human cytomegalovirus (HCMV) is a ubiquitous human herpes virus, which can infect varieties of cells including endothelial cells. Studies reported that the viral protein pUL135 is very important for virus replication, reactivation and immune escape. Therefore, we hypothesize that HCMV pUL135 may have a pathogenic effect on KD.
Methods:
We first determined pUL135 levels in the serum from KD patients. Next, we examined the effects and mechanisms of pUL135 on endothelial cell proliferation and migration. Finally, we assessed the effect of pUL135 on cardiac inflammation in a KD murine model.
Results:
Data showed that pUL135 level was significantly increased in the serum from KD patients compared with the healthy and fever controls. And pUL135 expression in endothelial cells remarkably inhibited cell proliferation, migration and tube formation. Moreover, expression of pUL135 obviously affected actin cytoskeleton. Mechanism investigation substantiated that pUL135 mediated endothelial cell dysfunction via regulating CD2AP. Ultimately, we found that HCMV pUL135 aggravated coronary arteritis in the Candida albicans cell wall extracts (CAWS)-induced KD mouse model.
Conclusion:
Our findings imply that HCMV pUL135-mediated endothelial dysfunction plays an important role in exacerbating coronary artery injury in KD conditions.
