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Cited by 94

The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Cigarette Smoke Exposure Attenuates Cytokine Production by Mouse Alveolar Macrophages

Gaschler, Gordon J., Zavitz, Caleb C. J., Bauer, Carla M. T., Skrtic, Marko, Lindahl, Maria, Robbins, Clinton S., Chen, Biao, Stämpfli, Martin R.·2008·American Journal of Respiratory Cell and Molecular Biology
DOI 10.1165/rcmb.2007-0053oc
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Abstract

Alveolar macrophages (aMϕs) play a central role in respiratory host defense by sensing microbial antigens and initiating immune-inflammatory responses early in the course of an infection. The purpose of this study was to investigate the effect of cigarette smoke exposure on aMϕs after stimulation of innate pattern recognition receptors (PRRs) in a murine model. To accomplish this, C57BL/6 mice were exposed for 8 weeks using two models of cigarette smoke exposure, nose-only or whole-body exposure, and aMϕs isolated from the bronchoalveolar lavage. After stimulation of aMϕs with pI:C, a mimic of viral replication, and bacterial cell-wall constituent LPS, aMϕs from cigarette smoke–exposed mice produced significantly attenuated levels of the inflammatory cytokines TNF-α and IL-6, and the chemokine RANTES. This attenuation was specific to the aMϕ compartment, and not related to changes in aMϕ viability or expression of Toll-like receptor (TLR)3 or TLR4 between groups. Furthermore, aMϕs from smoke-exposed mice had decreased cytokine RNA as compared with aMϕs from sham-exposed mice. Mechanistically, this was associated with decreased nuclear translocation of the proinflammatory transcription factor NF-κB, and increased activator protein-1 nuclear translocation, in aMϕs from smoke-exposed mice. Attenuated cytokine production was reversible after smoking cessation. Cigarette smoke exposure also attenuated TNF-α production after stimulation with nucleotide-oligomerization domain–like receptor agonists, showing that the effect applies more broadly to other PRR pathways. Our data demonstrate that cigarette smoke exposure attenuates aMϕ responses after innate stimulation, including pathways typically associated with bacterial and viral infections.

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Cited by

Metadata

Authors
Gaschler, G. J., Zavitz, C. C. J., Bauer, C. M. T., Skrtic, M., Lindahl, M., Robbins, C. S., Chen, B., & Stämpfli, M. R.
Venue
American Journal of Respiratory Cell and Molecular Biology
Publisher
Oxford University Press (OUP)
Published
2008-02-01
Volume
38
Issue
2
Pages
218-226
ISSN
  • 1044-1549
  • 1535-4989
DOI
10.1165/rcmb.2007-0053oc
Cited by
94
References
3
Language
en
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.