Citation

BibTex format

@article{Kirsebom:2019:10.1038/s41385-019-0190-0,
author = {Kirsebom, FCM and Kausar, F and Nuriev, R and Makris, S and Johansson, C},
doi = {10.1038/s41385-019-0190-0},
journal = {Mucosal Immunology},
pages = {1244--1255},
title = {Neutrophil recruitment and activation are differentially dependent on MyD88/TRIF and MAVS signaling during RSV infection},
url = {http://dx.doi.org/10.1038/s41385-019-0190-0},
volume = {12},
year = {2019}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections, especially in infants. Lung neutrophilia is a hallmark of RSV disease but the mechanism by which neutrophils are recruited and activated is unclear. Here, we investigate the innate immune signaling pathways underlying neutrophil recruitment and activation in RSV-infected mice. We show that MyD88/TRIF signaling is essential for lung neutrophil recruitment while MAVS signaling, leading to type I IFN production, is necessary for neutrophil activation. Consistent with that notion, administration of type I IFNs to the lungs of RSV-infected Mavs-/- mice partially activates lung neutrophils recruited via the MyD88/TRIF pathway. Conversely, lack of neutrophil recruitment to the lungs of RSV-infected Myd88/Trif-/- mice can be reversed by administration of chemoattractants and those neutrophils become fully activated. Interestingly, Myd88/Trif-/- mice did not have increased lung RSV loads during infection, suggesting that neutrophils are dispensable for control of the virus. Thus, two distinct pathogen sensing pathways collaborate for neutrophil recruitment and full activation during RSV infection.
AU - Kirsebom,FCM
AU - Kausar,F
AU - Nuriev,R
AU - Makris,S
AU - Johansson,C
DO - 10.1038/s41385-019-0190-0
EP - 1255
PY - 2019///
SN - 1933-0219
SP - 1244
TI - Neutrophil recruitment and activation are differentially dependent on MyD88/TRIF and MAVS signaling during RSV infection
T2 - Mucosal Immunology
UR - http://dx.doi.org/10.1038/s41385-019-0190-0
UR - http://hdl.handle.net/10044/1/71740
VL - 12
ER -