Sunday, 6th of March 2011 |
From the Journal of Infectious Diseases, ‘Cigarette smoke increases susceptibility to tuberculosis.’ Why is it that so few governments in Africa and Asia have declared war on tobacco, or even taken up arms against it? Why can I buy unfiltered cigarettes for a dollar a pack in most of Africa, where they would cost $10, with age screening, in most OECD countries? Who benefits by making premature death cheap and easy?
Full text is at http://jid.oxfordjournals.org/content/early/2011/02/22/infdis.jir009.full
From the discussion: In summary, we have shown in an in vivo model of M. tuberculosis infection that prior CS exposure impairs host defense against tuberculosis. We corroborated these findings in differentiated THP-1 human macrophages and primary human alveolar macrophages exposed to CS extract. Using both types of human macrophages, we showed that 2 of the major components of CS—nicotine and acrolein—likely play a role in the increased susceptibility to tuberculosis with CS exposure. These studies are the first (to our knowledge) to experimentally explain the biological mechanisms behind the epidemiological link between CS exposure and increased susceptibility to tuberculosis described in the literature. Future studies should examine the mechanisms by which acrolein, nicotine, and possibly other components of CS may be responsible for the enhanced susceptibility to tuberculosis. Since there is also strong epidemiological evidence that CS exposure increases the risk of reactivation tuberculosis, future studies should address a latent model of tuberculosis infection to determine whether CS increases susceptibility to reactivation tuberculosis.
Cigarette Smoke Increases Susceptibility to Tuberculosis—Evidence From In Vivo and In Vitro Models
1. Shaobin Shang1,a,
2. Diane Ordway1,a,
4. Xiyuan Bai2,4,
6. Crystal Shanley1,
7. Ian M. Orme1,
8. Stephanie Case3,
9. Maisha Minor3,
10. David Ackart1,
11. Laurel Hascall-Dove1,
12. Alida R. Ovrutsky2,4,
14. Dennis R. Voelker3,
15. Cherie Lambert5,
16. Brian M. Freed5,
17. Michael D. Iseman3,4,
18. Randall J. Basaraba1 and
19. Edward D. Chan2,3,4
+ Author Affiliations
1. 1Mycobacteria Research Laboratories, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins 2. 2Denver Veterans Affairs Medical Center 3. 3Departments of Medicine and Academic Affairs, National Jewish Health; and Divisions of 4. 4Pulmonary Sciences and Critical Care Medicine 5. 5Allergy and Clinical Immunology, University of Colorado Denver at Anschutz Medical Campus, Denver, Colorado1. Reprints or correspondence: Diane Ordway, PhD, Department of Microbiology, Immunology, and Pathology, Colorado State University, Fort Collins, CO 80523-1682 (d.ordway-rodriguez@colostate.edu).
Abstract
Background. Cigarette smoke (CS) exposure is an epidemiological risk factor for tuberculosis, although the biological basis has not been elucidated.
Methods. We exposed C57BL/6 mice to CS for 14 weeks and examined their ability to control an aerosol infection of Mycobacterium tuberculosis Erdman.
Results. CS-exposed mice had more M. tuberculosis isolated from the lungs and spleens after 14 and 30 d, compared with control mice. The CS-exposed mice had worse lung lesions and less lung and splenic macrophages and dendritic cells (DCs) producing interleukin12 and tumor necrosis factor α (TNF-α). There were significantly more interleukin 10–producing macrophages and DCs in the spleens of infected CS-exposed mice than in non-CS-exposed controls. CS-exposed mice also showed a diminished influx of interferon γ–producing and TNF-α-producing CD4+ and CD8+ effector and memory T cells into the lungs and spleens. There was a trend toward an increased number of viable intracellular M. tuberculosis in macrophages isolated from humans who smoke compared with nonsmokers. THP-1 human macrophages and primary human alveolar macrophages exposed to CS extract, nicotine, or acrolein showed an increased burden of intracellular M. tuberculosis.
Conclusion. CS suppresses the protective immune response to M. tuberculosis in mice, human THP-1 cells, and primary human alveolar macrophages.
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