In this section
@article{Harker:2014:10.1128/JVI.02620-13,
author = {Harker, JA and Yamaguchi, Y and Culley, FJ and Tregoning, JS and Openshaw, PJM},
doi = {10.1128/JVI.02620-13},
journal = {Journal of Virology},
title = {Delayed sequelae of neonatal RSV infection are dependent on cells of the innate immune system},
url = {http://dx.doi.org/10.1128/JVI.02620-13},
year = {2014}
}
TY - JOUR
AB - Infection with respiratory syncytial virus (RSV) in neonatal mice leads to exacerbated disease if mice are re-infected with the same virus as adults. Both T cells and host MHC genotype contribute to this phenomenon, but the part played by innate immunity has not been defined. Since macrophages and natural killer (NK) cells play key roles in regulating inflammation during RSV infection of adult mice, we studied the role of these cells in exacerbated inflammation following neonatal RSV sensitization/adult re-infection. Compared to those undergoing primary adult infection, neonatally sensitized mice showed enhanced airway fluid levels of interleukin-6 (IL-6), interferon alpha (IFNα), CXCL1 (KC) and tumor necrosis factor alpha (TNFα) at 12-24h, and IL-4, IL-5, IFNγ and CCL11 (eotaxin) at day 4 after re-infection. Weight loss during re-infection was accompanied by an initial influx of NK cells and granulocytes into the airways and lungs, followed by T cells. NK depletion during re-infection attenuated weight loss, but did not alter T cell responses. Depleting alveolar macrophages with inhaled clodronate liposomes reduced both NK and T cell numbers and attenuated weight loss. These findings indicate a hitherto unappreciated role for the innate immune response in governing the pathogenic recall responses to RSV infection.
AU - Harker,JA
AU - Yamaguchi,Y
AU - Culley,FJ
AU - Tregoning,JS
AU - Openshaw,PJM
DO - 10.1128/JVI.02620-13
PY - 2014///
SN - 0022-538X
TI - Delayed sequelae of neonatal RSV infection are dependent on cells of the innate immune system
T2 - Journal of Virology
UR - http://dx.doi.org/10.1128/JVI.02620-13
UR - http://doi.org/10.1128/JVI.02620-13
ER -