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Innate imprinting of murine resident alveolar macrophages by allergic bronchial inflammation causes a switch from hypoinflammatory to hyperinflammatory reactivity

Thomas Naessens UGent, Seppe Vander Beken UGent, Pieter Bogaert UGent, Nico Van Rooijen, Stefan Lienenklaus, Siegfried Weiss, Stefaan De Koker UGent and Johan Grooten UGent (2012) AMERICAN JOURNAL OF PATHOLOGY. 181(1). p.174-184
abstract
Resident alveolar macrophages (rAMs) residing in the bronchoalveolar lumen of the airways play an important role in limiting excessive inflammatory responses in the respiratory tract High phagocytic activity along with hyporesponsiveness to inflammatory insults and lack of autonomous IFN-beta production are crucial assets in this regulatory function. Using a mouse model of asthma, we analyzed the fate of rAMs both during and after allergic bronchial inflammation. Although nearly indistinguishable phenotypically from naive rAMs, postinflammation rAMs exhibited a strongly reduced basal phagocytic capacity, accompanied by a markedly increased inflammatory reactivity to Toll-like receptors TLR-3 (poly I:C), TLR-4 [lipopolysaccharide (LPS)], and TLR-7 (imiquimod). Importantly, after inflammation, rAMs exhibited a switch from an IFN-beta-defective to an IFN-beta-competent phenotype, thus indicating the occurrence of a new, inflammatory-released rAM population in the postallergic lung. Analysis of rAM turnover revealed a rapid disappearance of naive rAMs after the onset of inflammation. This inflammation-induced rAM turnover is critical for the development of the hyperinflammatory rAM phenotype observed after clearance of bronchial inflammation. These data document a novel mechanism of innate imprinting in which noninfectious bronchial inflammation causes alveolar macrophages to acquire a highly modified innate reactivity. The resulting increase in secretion of inflammatory mediators on TLR stimulation implies a role for this phenomenon of innate imprinting in the increased sensitivity of postallergic lungs to inflammatory insults. (Am J Pathol 2012, 181:174-184; http://dx.doi.org/10.1016/j.ajpath.2012.03.015)
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
RESPIRATORY-TRACT, PULMONARY DENDRITIC CELLS, ALTERNATIVE ACTIVATION, LUNG MACROPHAGES, IMMUNE-RESPONSE, MICE, DISEASE, ASTHMA, HETEROGENEITY, ELIMINATION
journal title
AMERICAN JOURNAL OF PATHOLOGY
Am. J. Pathol.
volume
181
issue
1
pages
174 - 184
Web of Science type
Article
Web of Science id
000305851100018
JCR category
PATHOLOGY
JCR impact factor
4.522 (2012)
JCR rank
10/77 (2012)
JCR quartile
1 (2012)
ISSN
0002-9440
DOI
10.1016/j.ajpath.2012.03.015
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2968115
handle
http://hdl.handle.net/1854/LU-2968115
date created
2012-08-06 12:42:04
date last changed
2012-08-10 09:46:27
@article{2968115,
  abstract     = {Resident alveolar macrophages (rAMs) residing in the bronchoalveolar lumen of the airways play an important role in limiting excessive inflammatory responses in the respiratory tract High phagocytic activity along with hyporesponsiveness to inflammatory insults and lack of autonomous IFN-beta production are crucial assets in this regulatory function. Using a mouse model of asthma, we analyzed the fate of rAMs both during and after allergic bronchial inflammation. Although nearly indistinguishable phenotypically from naive rAMs, postinflammation rAMs exhibited a strongly reduced basal phagocytic capacity, accompanied by a markedly increased inflammatory reactivity to Toll-like receptors TLR-3 (poly I:C), TLR-4 [lipopolysaccharide (LPS)], and TLR-7 (imiquimod). Importantly, after inflammation, rAMs exhibited a switch from an IFN-beta-defective to an IFN-beta-competent phenotype, thus indicating the occurrence of a new, inflammatory-released rAM population in the postallergic lung. Analysis of rAM turnover revealed a rapid disappearance of naive rAMs after the onset of inflammation. This inflammation-induced rAM turnover is critical for the development of the hyperinflammatory rAM phenotype observed after clearance of bronchial inflammation. These data document a novel mechanism of innate imprinting in which noninfectious bronchial inflammation causes alveolar macrophages to acquire a highly modified innate reactivity. The resulting increase in secretion of inflammatory mediators on TLR stimulation implies a role for this phenomenon of innate imprinting in the increased sensitivity of postallergic lungs to inflammatory insults. (Am J Pathol 2012, 181:174-184; http://dx.doi.org/10.1016/j.ajpath.2012.03.015)},
  author       = {Naessens, Thomas and Vander Beken, Seppe and Bogaert, Pieter and Van Rooijen, Nico and Lienenklaus, Stefan and Weiss, Siegfried and De Koker, Stefaan and Grooten, Johan},
  issn         = {0002-9440},
  journal      = {AMERICAN JOURNAL OF PATHOLOGY},
  keyword      = {RESPIRATORY-TRACT,PULMONARY DENDRITIC CELLS,ALTERNATIVE ACTIVATION,LUNG MACROPHAGES,IMMUNE-RESPONSE,MICE,DISEASE,ASTHMA,HETEROGENEITY,ELIMINATION},
  language     = {eng},
  number       = {1},
  pages        = {174--184},
  title        = {Innate imprinting of murine resident alveolar macrophages by allergic bronchial inflammation causes a switch from hypoinflammatory to hyperinflammatory reactivity},
  url          = {http://dx.doi.org/10.1016/j.ajpath.2012.03.015},
  volume       = {181},
  year         = {2012},
}

Chicago
Naessens, Thomas, Seppe Vander Beken, Pieter Bogaert, Nico Van Rooijen, Stefan Lienenklaus, Siegfried Weiss, Stefaan De Koker, and Johan Grooten. 2012. “Innate Imprinting of Murine Resident Alveolar Macrophages by Allergic Bronchial Inflammation Causes a Switch from Hypoinflammatory to Hyperinflammatory Reactivity.” American Journal of Pathology 181 (1): 174–184.
APA
Naessens, T., Vander Beken, S., Bogaert, P., Van Rooijen, N., Lienenklaus, S., Weiss, S., De Koker, S., et al. (2012). Innate imprinting of murine resident alveolar macrophages by allergic bronchial inflammation causes a switch from hypoinflammatory to hyperinflammatory reactivity. AMERICAN JOURNAL OF PATHOLOGY, 181(1), 174–184.
Vancouver
1.
Naessens T, Vander Beken S, Bogaert P, Van Rooijen N, Lienenklaus S, Weiss S, et al. Innate imprinting of murine resident alveolar macrophages by allergic bronchial inflammation causes a switch from hypoinflammatory to hyperinflammatory reactivity. AMERICAN JOURNAL OF PATHOLOGY. 2012;181(1):174–84.
MLA
Naessens, Thomas, Seppe Vander Beken, Pieter Bogaert, et al. “Innate Imprinting of Murine Resident Alveolar Macrophages by Allergic Bronchial Inflammation Causes a Switch from Hypoinflammatory to Hyperinflammatory Reactivity.” AMERICAN JOURNAL OF PATHOLOGY 181.1 (2012): 174–184. Print.