Cigarette Smoke Damages White Blood Cells

The hazards of smoking are well documented, but results of a recent study published in BMC Cell Biology sheds new light on what happens to neutrophils, white blood cells responsible for destruction of microbial invaders, when they are persistently exposed to cigarette smoke, and provides evidence of the increased susceptibility of smokers to bacterial infections. Previous studies have examined the influence of tobacco smoke and its components on neutrophil function. This one was the first of its kind to examine the effect of nicotine exposure on neutrophils during their developmental, or differentiation stage. Results of the study showed that neutrophils exposed to nicotine can lose their ability to kill bacteria, and often increase their expression of an enzyme associated with certain cancers.

Neutrophils circulating in the bloodstream are central to the body's defense against bacterial infection. Like all blood cells, neutrophils originate in the bone marrow, as common stem cells, and then differentiate to become neutrophils, or some other type of blood cell, in the process known as hematopoiesis. Although cigarette smoke contains over 4000 different compounds, the authors of this study focused on the effects of nicotine, because it is a major component of tobacco smoke, and because neutrophils express nicotine receptors on their surface. Previous studies have shown that nicotine receptor levels are higher in the neutrophils of smokers, and decline when smokers quit. Nicotine concentration in the blood of smokers is high, and even higher in tissues of the arteries, lungs, and mouth. Gum, patches, and sprays for the purpose of aiding smokers in their efforts to quit, by providing a system of periodic nicotine delivery have been shown to actually hamper neutrophil repair. Smoking causes a condition known as systemic neutrophilia, or leukocytosis, indicated by an increased number of neutrophils in blood and tissues. This condition can lead to cardiovascular diseases, asthma, periodontal (gum) disease, and an increased risk of infectious diseases such as tuberculosis, meningitis, and other bacterial infections. Previous studies have established that tobacco smoke affects neutrophil function. Prior to this study, however, little was known about the effects of tobacco smoke on neutrophils prior to leaving the bone marrow.

Results of the study demonstrated that nicotine does not influence neutrophil structure or viability, but does affect certain functions, such as bacterial killing, and increases the release of MMP-9, an enzyme whose overproduction is associated with tumor formation. The authors reported that in addition, nicotine altered the protein content of neutrophils, but more research will be required for a better understanding of why this happens. The authors used the pathogen Porphyromonas gingivalis, a bacterial species implicated in certain types of dental infection, to demonstrate nicotine's effect on the oxidative burst, a mechanism used by neutrophils to destroy microbial invaders. Neutrophils exposed to nicotine had a reduced ability to employ an oxidative burst to destroy and engulf P. gingivalis.

Chronic smoking increases the risk of a multitude of illnesses. The study outlined here provides new details on the effect of nicotine on neutrophil activity, and protein expression. Further studies may include experiments with other components of tobacco smoke. Results like these are difficult to ignore, because they help to provide an increasingly detailed picture of the damage to neutrophils by prolonged exposure to tobacco smoke. Neutrophils are intricately designed by nature to defend against bacterial infection, and cigarette smoke clearly makes that job much more difficult.

Xu, M., Scott, J., Liu, K., Bishop, H., Renaud, D., Palmer, R., Soussi-Gounni, A., Scott, D.

The influence of nicotine on granulocytic differentiation-Inhibition of the oxidative burst and bacterial killing and increased matrix metalloproetinase-9 release

http://www.biomedcentral.com/1471-2121/9/19