BibTex format
@misc{Peel,
author = {Peel, T and Jackson, D and Johnston, S and Walton, R},
title = {IL-23, Increased In Asthmatics, Licences IL-17 Secretion In Response To Rhinovirus Infection},
type = {Poster},
}
In this section
@misc{Peel,
author = {Peel, T and Jackson, D and Johnston, S and Walton, R},
title = {IL-23, Increased In Asthmatics, Licences IL-17 Secretion In Response To Rhinovirus Infection},
type = {Poster},
}
TY - GEN
AB - : While the main axis of allergic inflammation in asthmatics has been considered Th2-driven eosinophilia and IgE, recentRATIONALEobservations have shown that, especially in moderate-to-severe asthmatics, IL-17 and neutrophils may also significantly contribute todisease. The cytokine IL-23, produced by dendritic cells and macrophages, is a main driver of IL-17 responses from T helper, γδ and innatelymphoid cells and has been shown to be increased in the serum of asthmatic subjects.The greatest clinical burden of asthma is associated with exacerbations, the majority of which are induced by rhinovirus. Rhinovirusinfection recruits significantly higher levels of neutrophils into the airways of asthmatics compared to healthy controls, which correlatewith loss of lung function. In addition, we have recently observed that IL-17 is higher in the airways of asthmatics both at baseline andfollowing experimental rhinovirus infection.We hypothesise that the presence of IL-23 drives IL-17 responses to rhinovirus, leading to increased neutrophilia andHYPOTHESIS:worsened lung function.: C57BL/6 mice were infected intranasally with rhinovirus serotype 1B. Neutrophils were recruited by 8 hoursMETHODS AND RESULTSand peaked at 24 hours, while CD4 IFNγ Th1 cells were recruited by day 7. Unlike in human subjects, no IL-17 responses to rhinovirus+ +were seen by ELISA, flow or qPCR. To investigate the effect of IL-23, infection was supplemented with 1µg of recombinant IL-23 (rIL-23).Alone, rIL-23 had no effect but elicited significant levels of IL-17 (mean 290pg/ml) and IL-17F (1917pg/ml) in the airways following arhinovirus infection. IL-17 secretion was associated with significant increases in airway neutrophilia (3-fold increase, <0.001). Additionally,Pinfection with rhinovirus caused increased persistence of rIL-23 in the airways 24 hours after infection compared to rIL-23 dosing alone (97vs. 660 pg/ml, <0.001).PIn the mouse, approximately two-thirds of &
AU - Peel,T
AU - Jackson,D
AU - Johnston,S
AU - Walton,R
TI - IL-23, Increased In Asthmatics, Licences IL-17 Secretion In Response To Rhinovirus Infection
ER -