Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette-smoke-induced lung inflammation in mice
Steven Bozinovski, Huei Jiunn Seow, Sheau Pyng Jamie Chan, Desiree Anthony, Jonathan McQualter, Michelle Hansen, Brendan J Jenkins, Gary P Anderson, Ross Vlahos
CLINICAL SCIENCE | PORTLAND PRESS LTD | Published : 2015
Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) is a pivotal cytokine that regulates lung immunity and inflammation. The aim of the present study was to investigate how IL-17A regulates CS-induced lung inflammation in vivo. IL-17A knockout (KO) mice and neutralization of IL-17A in wild-type (WT) mice reduced macrophage and neutrophil recruitment and chemokine (C-C motif) ligand 2 (CCL2), CCL3 and matrix metalloproteinase (MMP)-12 mRNA expression in response to acute CS exposure. IL-17A expression was increased in non-obese diabetic (NOD) severe combined immunodeficiency SCID) mice with non-functional B- and T-cells over a 4-we..View full abstract
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Awarded by National Health and Medical Research Council of Australia
This work was supported by the National Health and Medical Research Council of Australia [grant number ID 1027112]; and the Operational Infrastructure Support Program by the Victorian Government of Australia.