Journal article
Respiratory Syncytial Virus Synergizes with Th2 Cytokines to Induce Optimal Levels of TARC/CCL17
The Journal of immunology (1950), Vol.179(3), pp.1648-1658
08/01/2007
DOI: 10.4049/jimmunol.179.3.1648
PMCID: PMC4060898
PMID: 17641031
Abstract
Respiratory syncytial virus (RSV) is a ubiquitous virus that preferentially infects airway epithelial cells causing asthma exacerbations and severe disease in immunocompromised hosts. Acute RSV infection induces inflammation in the lung. The chemokine, TARC, recruits Th2 cells to sites of inflammation. We found that acute RSV infection of BALB/c mice increased TARC production in the lung. Immunization of BALB/c mice with individual RSV proteins can lead to the development of Th1 or Th2 biased T cell responses in the lung following RSV infection. We primed animals with a recombinant vaccinia virus (vv) expressing either the RSV fusion (F) protein or the RSV attachment (G) protein, inducing Th1- and Th2-biased pulmonary memory T cell responses, respectively. After RSV infection, TARC production significantly increased in the vvG primed animals only. These data suggest a positive feedback loop for TARC production between RSV infection and Th2 cytokines. RSV infected lung epithelial cells cultured with IL-4 or IL-13 demonstrated a marked increase in the production of TARC. The synergistic effect of RSV and IL-4/ IL-13 on TARC production reflected differential induction of NFκB and STAT6 by the two stimuli (both are in the TARC promoter). These findings demonstrate that RSV induces a chemokine TARC that has the potential to recruit Th2 cells to the lung.
Details
- Title: Subtitle
- Respiratory Syncytial Virus Synergizes with Th2 Cytokines to Induce Optimal Levels of TARC/CCL17
- Creators
- Martha M Monick - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IALinda S Powers - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IAIhab Hassan - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IADayna Groskreutz - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IATimur O Yarovinsky - Department of Immunobiology, Yale University, New Haven, CTChristopher W Barrett - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IAElaine M Castilow - Department of Microbiology, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IADelia Tifrea - Department of Interdisciplinary Graduate Program in Immunology, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IASteven M Varga - Department of Microbiology, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IAGary W Hunninghake - Department of Internal Medicine, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IA
- Resource Type
- Journal article
- Publication Details
- The Journal of immunology (1950), Vol.179(3), pp.1648-1658
- DOI
- 10.4049/jimmunol.179.3.1648
- PMID
- 17641031
- PMCID
- PMC4060898
- NLM abbreviation
- J Immunol
- ISSN
- 0022-1767
- eISSN
- 1550-6606
- Language
- English
- Date published
- 08/01/2007
- Academic Unit
- Pulmonary, Critical Care, and Occupational Medicine; Graduate College Admin and Gen; Microbiology and Immunology; Pathology; Internal Medicine
- Record Identifier
- 9984083243202771
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