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,
,
Departments of
* Internal Medicine and
Microbiology and
Interdisciplinary Graduate Program in Immunology, University of Iowa Carver College of Medicine and Veterans Administration Medical Center, Iowa City, IA 52242; and
Department of Immunobiology, Yale University, New Haven, CT 06510
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. Thymus- and activation-regulated 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 after RSV infection. We primed animals with a recombinant vaccinia virus 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 vaccinia virus G-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 NF
B 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.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported by a Veterans Administration Merit Review Grant and by National Institutes of Health Grants AI063502 (to S.M.V.), HL-60316, HL-077431, HL079901-01A1 (to G.W.H.), and RR00059 from the General Clinical Research Centers Program, National Center for Research Resources, National Institutes of Health.
2 Address correspondence and reprint requests to Dr. Martha M. Monick, Division of Pulmonary, Critical Care, and Occupational Medicine, Room 100, Eckstein Medical Research Building, Carver College of Medicine, University of Iowa, Iowa City, IA 52242. E-mail address: martha-monick{at}uiowa.edu
3 Abbreviations used in this paper: RSV, respiratory syncytial virus; HPRT, hypoxanthine guanine phosphoribosyl transferase; IP-10/CXCL10, human IFN-inducible protein 10; moi, multiplicity of infection; PI, propidium iodide; qRT-PCR, quantitative RT-PCR; TARC/CCL17, thymus- and activation-regulated chemokine; PVDF, polyvinylidene difluoride; CBP, CREB-binding protein.
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