IL-17A and serum amyloid A are elevated in a cigarette smoke cessation model associated with the persistence of pigmented macrophages, neutrophils and activated NK cells

Hansen, M, Chan, S, Langenbach, S, Dousha, L, Jones, J, Yatmaz, S, Seow, H, Vlahos, R, Anderson, G and Bozinovski, S 2014, 'IL-17A and serum amyloid A are elevated in a cigarette smoke cessation model associated with the persistence of pigmented macrophages, neutrophils and activated NK cells', PLoS One, vol. 9, no. 11, e113180, pp. 1-11.


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Title IL-17A and serum amyloid A are elevated in a cigarette smoke cessation model associated with the persistence of pigmented macrophages, neutrophils and activated NK cells
Author(s) Hansen, M
Chan, S
Langenbach, S
Dousha, L
Jones, J
Yatmaz, S
Seow, H
Vlahos, R
Anderson, G
Bozinovski, S
Year 2014
Journal name PLoS One
Volume number 9
Issue number 11
Article Number e113180
Start page 1
End page 11
Total pages 11
Publisher Public Library of Science
Abstract While global success in cessation advocacy has seen smoking rates fall in many developed countries, persistent lung inflammation in ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, candidate effector mechanisms were assessed in mice exposed to cigarette smoke (CS) for 4 months following cessation from long term CS exposure. BALF neutrophils, CD4+ and CD8+ T cells and lung innate NK cells remained significantly elevated following smoking cessation. Analysis of neutrophil mobilization markers showed a transition from acute mediators (MIP-2α, KC and G-CSF) to sustained drivers of neutrophil and macrophage recruitment and activation (IL-17A and Serum Amyoid A (SAA)). Follicle-like lymphoid aggregates formed with CS exposure and persisted with cessation, where they were in close anatomical proximity to pigmented macrophages, whose number actually increased 3-fold following CS cessation. This was associated with the elastolytic protease, MMP-12 (macrophage metallo-elastase) which remained significantly elevated post-cessation. Both GM-CSF and CSF-1 were significantly increased in the CS cessation group relative to the control group. In conclusion, we show that smoking cessation mediates a transition to accumulation of pigmented macrophages, which may contribute to the expanded macrophage population observed in COPD. These macrophages together with IL-17A, SAA and innate NK cells are identified here as candidate persistence determinants and, we suggest, may represent specific targets for therapies directed towards the amelioration of chronic airway inflammation.
Subject Respiratory Diseases
Clinical Sciences not elsewhere classified
Keyword(s) amyloid A protein
CXCL1 chemokine
CXCL2 chemokine
granulocyte macrophage colony stimulating factor
interleukin 10
interleukin 17
interleukin 23
interleukin 6
macrophage elastase
messenger RNA
DOI - identifier 10.1371/journal.pone.0113180
Copyright notice © 2014 Hansen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
ISSN 1932-6203
Additional Notes Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
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