PMID- 20205592
OWN - NLM
STAT- MEDLINE
DCOM- 20100408
LR  - 20181113
IS  - 1537-6613 (Electronic)
IS  - 0022-1899 (Print)
IS  - 0022-1899 (Linking)
VI  - 201
IP  - 8
DP  - 2010 Apr 15
TI  - Respiratory syncytial virus F and G proteins induce interleukin 1alpha, CC, and 
      CXC chemokine responses by normal human bronchoepithelial cells.
PG  - 1201-7
LID - 10.1086/651431 [doi]
AB  - Human respiratory syncytial virus (RSV) is a ubiquitous respiratory virus that 
      causes serious lower respiratory tract disease in infants and young children 
      worldwide. Studies have shown that RSV infection modulates chemokine expression 
      patterns, suggesting that particular cytokine expression profiles may be 
      indicators of disease severity. In this study, we show that RSV F or G protein 
      treatment of fully differentiated primary normal human bronchial epithelial cells 
      induces apical and basolateral secretion of interleukin 8 (IL-8), 
      interferon-inducible protein 10 (IP-10), monocyte chemotactic protein 1 (MCP-1), 
      and RANTES (regulated on activation, normal T cell expressed and secreted). 
      Purified RSV G (attachment) protein was shown to stimulate the secretion of 
      interleukin 1alpha and RANTES, whereas purified F (fusion) protein elicited the 
      production of IL-8, IP-10, and RANTES. Studies of ultraviolet-inactivated RSV 
      showed that treatment of normal human bronchial epithelial cells induces apical 
      IL-8, IP-10, and MCP-1 secretion independent of infection, suggesting that RSV 
      proteins alone modify the chemokine response pattern, which may affect the early 
      immune response before infection.
FAU - Oshansky, Christine M
AU  - Oshansky CM
AD  - Department of Infectious Diseases, College of Veterinary Medicine, Center for 
      Disease Intervention, University of Georgia, Athens, Georgia 30602, USA.
FAU - Barber, James P
AU  - Barber JP
FAU - Crabtree, Jackelyn
AU  - Crabtree J
FAU - Tripp, Ralph A
AU  - Tripp RA
LA  - eng
GR  - R01 AI069275/AI/NIAID NIH HHS/United States
GR  - R01 AI069275-03/AI/NIAID NIH HHS/United States
GR  - R01 AI088744/AI/NIAID NIH HHS/United States
GR  - R01-AI069275-03/AI/NIAID NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Infect Dis
JT  - The Journal of infectious diseases
JID - 0413675
RN  - 0 (Chemokine CXCL10)
RN  - 0 (Chemokines, CC)
RN  - 0 (Chemokines, CXC)
RN  - 0 (F protein, human respiratory syncytial virus)
RN  - 0 (G glycoprotein, Respiratory syncytial virus)
RN  - 0 (Interleukin-1alpha)
RN  - 0 (Interleukin-8)
RN  - 0 (Viral Fusion Proteins)
SB  - IM
MH  - Adolescent
MH  - Bronchi/immunology/*virology
MH  - Cells, Cultured
MH  - Chemokine CXCL10/biosynthesis
MH  - Chemokines, CC/*biosynthesis
MH  - Chemokines, CXC/*biosynthesis
MH  - Epithelium/immunology/virology
MH  - Gene Expression Regulation, Viral/physiology
MH  - Humans
MH  - Interleukin-1alpha/*biosynthesis
MH  - Interleukin-8/biosynthesis
MH  - Male
MH  - Respiratory Syncytial Virus Infections/immunology
MH  - Respiratory Syncytial Viruses/immunology
MH  - Viral Fusion Proteins/*pharmacology
PMC - PMC2839062
MID - NIHMS171917
COIS- The authors do not have a commercial or other association that might pose a 
      conflict of interest.
EDAT- 2010/03/09 06:00
MHDA- 2010/04/09 06:00
PMCR- 2011/04/15
CRDT- 2010/03/09 06:00
PHST- 2010/03/09 06:00 [entrez]
PHST- 2010/03/09 06:00 [pubmed]
PHST- 2010/04/09 06:00 [medline]
PHST- 2011/04/15 00:00 [pmc-release]
AID - 10.1086/651431 [doi]
PST - ppublish
SO  - J Infect Dis. 2010 Apr 15;201(8):1201-7. doi: 10.1086/651431.