Cigarette smoke exacerbates alcohol's effects on defense against Streptococcus pneumoniae

May 15, 2005

Streptococcus pneumoniae is a bacterium that can infect the upper respiratory tract and cause pneumonia, as well as infections in other parts of the body such as the bloodstream (bacteremia), lining of the brain and spinal cord (meningitis), bones (osteomyelitis), joints (arthritis), ears (otitis media) and sinuses (sinusitis). Alcoholics and cigarette smokers are particularly susceptible to pulmonary infections caused by S. pneumoniae. A rodent study in the May issue of Alcoholism: Clinical & Experimental Research has found that alcohol consumption increases movement of S. pneumoniae toward the lungs, and that smoke exposure exacerbates the alcohol-induced increase in bacterial penetration.

"All of the infections caused by S. pneumoniae start with the bacterium colonizing or binding to cells in the upper part of the nose, which is called the nasopharynx," said Gentry-Nielsen, professor of microbiology and immunology at Creighton University School of Medicine, research microbiologist at the Omaha Veterans Affairs Medical Center, and corresponding author for the study. "The trachea that leads from the nasopharynx to the lungs is lined with cells that have hair-like projections called cilia. These cilia beat in an upward direction to sweep mucus and microorganisms like S. pneumoniae upward and prevent their movement into the lungs. Disease normally occurs when the immune system is compromised or the person is colonized with a new or especially virulent strain of S. pneumoniae that is able to evade the action of the cilia and travel from the nasopharynx into the lungs."

Gentry-Nielsen said that alcoholics are more susceptible to S. pneumoniae infections for several reasons. "They have a decreased gag reflex and an increased risk of movement of nasopharyngeal and gastric contents into their lungs, especially when they lose consciousness," she said. "Both of these defects provide additional opportunities for S. pneumoniae to enter their lungs. Host defenses within the lungs of alcoholics are also compromised, so they are not well equipped to handle the infection once the organisms reach the lungs. Cigarette smokers also have an increased susceptibility to pulmonary infections caused by S. pneumoniae. Smokers are much more likely to be colonized with the organism in their mouths and nasopharynx than non-smokers. Smoking also injures cilia and alters the efficiency of their beating so that bacteria entering the trachea have an increased likelihood of making their way into the lungs."

"Clinical studies of this type are complicated because at least 80 percent of human alcoholics smoke," added Gregory J. Bagby, Kai and Earl Rozas professor of physiology at Louisiana State University Health Sciences Center. "Controlled studies in animals are therefore critically important in identifying interactive and separate effects of these two agents. This group is one of the first to study this interaction in a systematic way and the present study on the interactive effects of cigarette smoke and alcohol on the mucociliary apparatus is the first study of its kind to my knowledge."

For 12 weeks, researchers exposed Sprague-Dawley rats (n=64) twice daily to either smoke generated from 30 cigarettes or room air. For the last five weeks of exposure, rats were fed liquid diets that contained 0, 16, 26 or 36 percent of their calories as alcohol. The rats were then infected intranasally with S. pneumoniae, and movement of the organisms into the lower respiratory tract was followed.

Results indicate that alcohol ingestion results in a dose-dependent increase in movement of S. pneumoniae into the rats' lungs, which is further exacerbated by concurrent smoke exposure.

"Our study is the first to have reported showing that alcohol consumption in rats impairs the beating of their tracheal cilia, and that this correlates with increased movement of S. pneumoniae into their lungs," said Gentry-Nielsen. "This alcohol-induced defect was intensified in smoke-exposed animals, although smoke exposure without ethanol ingestion did not increase movement of organisms into the lungs. These results point to alcohol- and smoke-induced defects in ciliary beating that are likely to make hosts more susceptible to infections caused by microorganisms that colonize their upper respiratory tracts."

"This study points to the importance of understanding the potential combined adverse effects of alcoholism and cigarette smoking on lung defenses against pathogen infection," added Bagby. "It also illustrates the difficulty of studying combined effects of alcohol consumption and cigarette smoke exposure on lung host defense. Although the study identifies a potential adverse effect of the combined insult of alcohol consumption and smoke exposure on bacterial burden in the lower respiratory tract, the small sample size precluded definitive conclusions from being made on this adverse effect. Future studies are needed to both describe the effects of alcohol and cigarette smoking on lung-host defense as well as the mechanisms involved."

Gentry-Nielsen and her colleagues plan to continue testing the effects of smoking and drinking on other aspects of defense against S. pneumoniae infections, including examination of an anti-asthma drug that decreases binding of S. pneumoniae to epithelial cells, and treatment with an agent that stimulates ciliary beating.
Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Smoke Exposure Exacerbates an Ethanol-Induced Defect in Mucociliary Clearance of Streptococcus Pneumoniae," were Elizabeth A. Vander Top and Todd A. Wyatt of the Veterans Affairs Medical Center in Omaha, Nebraska. The study was funded by the National Institutes of Health, and the National Institute on Alcohol Abuse and Alcoholism.

Alcoholism: Clinical & Experimental Research

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