In vitro response of immunoregulatory cytokine expression in human monocytic cells to human parvovirus B19 capsid.
Human parvovirus B19 is a clinically important pathogen in both children and adults. In adults, it frequently causes acute and chronic arthritis, which may be related to persistent infection. The effect of the capsid of human parvovirus B19 on monocytes, which are thought to be responsible for the first line of defense against parvoviral infection, is not well understood. In this study, we investigated changes in mRNA expression levels of several immunoregulatory cytokines in monocytic cells after treatment with the B19 capsid. When human monocytic cell line THP-1 cells were treated with the B19 capsid, the expression of tumor necrosis factor alpha (TNF-alpha) mRNA was suppressed independently of transforming growth factor beta (TGF-beta) mRNA. In contrast, the level of mRNA for interleukin-1 alpha (IL-1alpha) remained unchanged, and that for interleukin-1 beta (IL-1beta) was slightly increased after the capsid treatment. Flow cytometry demonstrated that THP-1 cells treated with B19 capsid showed no differences in surface expression of CD11a, CD16 and CD33, as compared with control cells. These findings that B19 capsid antigen did not promote positive responses for production of TNF-alpha and IL-1alpha may provide insight into the mechanisms of persistent infection of human parvovirus B19 and the systemic viral spread via bloodstream.
Fujita
Tetsuhiro
T
Department of Pharmacotherapeutics, Showa Pharmaceutical University, 3-3165 Higashitamagawagakuen, Machida, Tokyo, Japan.
Ikejima
Hideaki
H
Yamagata
Nanako
N
Kudo
Yuko
Y
Hoshi
Keiko
K
D036022:Capsid Proteins / Q000494:pharmacology*; D002460:Cell Line; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005434:Flow Cytometry; D006801:Humans; D066298:In Vitro Techniques; D053582:Interleukin-1alpha / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D016732:Parvovirus B19, Human / Q000276:immunology*; D012333:RNA, Messenger / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
D036022:Capsid Proteins; D016207:Cytokines; D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; C095547:capsid protein VP1, parvovirus B19; C095548:capsid protein VP2, parvovirus B19