TY - JOUR
T1 - Comprehensive analysis of serum cytokines/chemokines in febrile children with primary human herpes virus-6B infection
AU - Nagasaka, Miwako
AU - Morioka, Ichiro
AU - Kawabata, Akiko
AU - Yamagishi, Yoshiaki
AU - Iwatani, Sota
AU - Taniguchi-Ikeda, Mariko
AU - Ishida, Akihito
AU - Iijima, Kazumoto
AU - Mori, Yasuko
N1 - Funding Information:
All authors have no financial relationships relevant to this article to disclose. Outside the submitted work, Ichiro Morioka has received grants from Japan Blood Product Organization , Daiichi Sankyo Co., Ltd. , MSD AbbVie LLC , Taisho Toyama Pharmaceutical Co., Ltd. , and Air Water Inc. ; lecture fees from MSD, Pfizer Japan, Inc. , Novo Nordisk Pharma Ltd. , Eli Lilly Japan K.K., Shionogi Co., Ltd. , AbbVie LLC, Japan Vaccine Co., Ltd. , KYORIN Pharmaceutical Co., Ltd. , and Atom Medical Corp. ; and consulting fees from Atom Medical Corp. , Sanofi K.K. , and Japan Blood Product Organization . Kazumoto Iijima has received grants from Pfizer Japan, Inc. , Daiichi Sankyo Co., Ltd. , Japan Blood Product Organization , Miyarisan Pharmaceutical Co., Ltd. , AbbVie LLC , CSL Behring , JCR Pharmaceuticals Co., Ltd. , and Teijin Pharma Ltd. ; lecture fees from MSD , ALEXION Pharmaceuticals , AstraZeneca K.K. , Meiji Seika Pharma Co., Ltd. , Novartis Pharma K.K. , Zenyaku Kogyo Co., Ltd. , Chugai Pharmaceutical Co., Ltd. , Astellas Pharma Inc. , Daiichi Sankyo, Co., Ltd. , Springer Japan , Asahi Kasei Pharma Corp , Boehringer Ingelheim , and Medical Review Co., Ltd. ; manuscript fees from Chugai Pharmaceutical Co., Ltd. ; and consulting fees from Chugai Pharmaceutical Co., Ltd. , Astellas Pharma Inc. , and Takeda Pharmaceutical Company Ltd .
Funding Information:
This work was supported by Grants-in-Aid for Scientific Research (B) (grant number: 24390114 , Y.M.), Scientific Research (C) (grant number: 26461632 , I.M.), and Young Scientists (B) (grant number: 15K19613 , M.N.) of JSPS KAKENHI.
PY - 2016/9/1
Y1 - 2016/9/1
N2 - Cytokines and chemokines induced by primary human herpes virus (HHV)-6B infection may play a critical role in the clinical manifestations of infection. In this study, we analyzed 40 cytokines/chemokines in febrile children with primary HHV-6B infection. Blood samples from 233 febrile and 36 afebrile patients 0–3 years of age were used for this study. In febrile patients, primary HHV-6B infection was determined by detection of HHV-6B DNA without anti-HHV-6 immunoglobulin G in the blood (HHV-6B group). Infection by other pathogens was assumed when HHV-6B DNA was not detected in the blood (non-HHV-6B group). Of the 233 febrile patients, 30 patients (13%) were diagnosed with primary HHV-6B infection. To analyze serum cytokines/chemokines, patients were randomly chosen from the HHV-6B (n = 25) and non-HHV-6B groups (n = 8). Sera from 25 afebrile patients were used as a control. When comparing the levels of 40 cytokines/chemokines between the HHV-6B and control groups, we found that four chemokines (chemokine [C-X-C motif] ligand [CXCL] 11, CXCL10, CXCL16, and chemokine [C-C motif] ligand [CCL] 2) were significantly upregulated in the HHV-6B group compared with those in the control. Of these, only CXCL11 levels were significantly higher in the HHV-6B group than in the non-HHV-6B group. Because the induction of CCL2 was already reported in an early study, we found, for the first time, the induction of three new chemokines, i.e., CXCL11, CXCL10, and CXCL16 in patients with primary HHV-6B infection. Importantly, we demonstrated that serum CXCL11 levels increased specifically in patients with HHV-6B infection.
AB - Cytokines and chemokines induced by primary human herpes virus (HHV)-6B infection may play a critical role in the clinical manifestations of infection. In this study, we analyzed 40 cytokines/chemokines in febrile children with primary HHV-6B infection. Blood samples from 233 febrile and 36 afebrile patients 0–3 years of age were used for this study. In febrile patients, primary HHV-6B infection was determined by detection of HHV-6B DNA without anti-HHV-6 immunoglobulin G in the blood (HHV-6B group). Infection by other pathogens was assumed when HHV-6B DNA was not detected in the blood (non-HHV-6B group). Of the 233 febrile patients, 30 patients (13%) were diagnosed with primary HHV-6B infection. To analyze serum cytokines/chemokines, patients were randomly chosen from the HHV-6B (n = 25) and non-HHV-6B groups (n = 8). Sera from 25 afebrile patients were used as a control. When comparing the levels of 40 cytokines/chemokines between the HHV-6B and control groups, we found that four chemokines (chemokine [C-X-C motif] ligand [CXCL] 11, CXCL10, CXCL16, and chemokine [C-C motif] ligand [CCL] 2) were significantly upregulated in the HHV-6B group compared with those in the control. Of these, only CXCL11 levels were significantly higher in the HHV-6B group than in the non-HHV-6B group. Because the induction of CCL2 was already reported in an early study, we found, for the first time, the induction of three new chemokines, i.e., CXCL11, CXCL10, and CXCL16 in patients with primary HHV-6B infection. Importantly, we demonstrated that serum CXCL11 levels increased specifically in patients with HHV-6B infection.
UR - http://www.scopus.com/inward/record.url?scp=84992645526&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84992645526&partnerID=8YFLogxK
U2 - 10.1016/j.jiac.2016.05.010
DO - 10.1016/j.jiac.2016.05.010
M3 - Article
C2 - 27346377
AN - SCOPUS:84992645526
VL - 22
SP - 593
EP - 598
JO - Journal of Infection and Chemotherapy
JF - Journal of Infection and Chemotherapy
SN - 1341-321X
IS - 9
ER -