The Effects of Chronic Ethanol Ingestion and Smoke Exposure on Anti-Pneumococcal Host Defenses
type: CreativeWork
description: Individuals who abuse alcohol and tobacco are at increased risk for pneumonia caused by Streptococcus pneumoniae (the pneumococcus). Alcohol and cigarette smoke are known to exert immunosuppressive effects on pulmonary defense mechanisms that protect the host from pneumococcal pneumonia. However, the interactive, combined immunosuppressive effects of ethanol (EtOH) ingestion and smoke exposure remain ill defined. To study these effects, we used a rat model that mimics chronic alcohol abuse and smoking. Rats were exposed to smoke generated by 30 reference cigarettes for one hour twice daily for 12 weeks or to room air (sham-exposed). During the last five weeks of exposure, the rats were pair-fed equal volumes of liquid diet containing 0% or 36% EtOH calories. Nasopharyngeal colonization was unaltered by EtOH ingestion and/or smoke exposure. The movement of pneumococci from the rats’ nasopharynx into the lungs was slightly increased by EtOH ingestion, but EtOH did not impair ciliary beating. Smoke exposure reduced pneumococcal movement into the lungs regardless of diet, and this was correlated with a significant increase in ciliary beat frequency. The effect of concurrent smoke exposure and EtOH ingestion on non-neutrophil (PMN)-mediated killing of pneumococci was investigated using an in vivo bactericidal assay. EtOH ingestion significantly decreased the percentage of pneumococci killed within the rats’ lungs. Unexpectedly, this EtOH-induced defect was counteracted by concurrent smoke exposure, even though smoke exposure alone did not increase intrapulmonary pneumococcal clearance. Quantification of the bactericidal proteins lysozyme and lactoferrin in the rats’ lungs did not explain the differences in non-PMN-mediated killing. However, EtOH-fed rats that were sham-exposed exhibited suppressed alveolar macrophage phagocytosis of pneumococci as well as diminished opsonization of the bacteria within their lungs. It is uncertain if smoke exposure increased macrophage ph…
abstract: Individuals who abuse alcohol and tobacco are at increased risk for pneumonia caused by Streptococcus pneumoniae (the pneumococcus). Alcohol and cigarette smoke are known to exert immunosuppressive effects on pulmonary defense mechanisms that protect the host from pneumococcal pneumonia. However, the interactive, combined immunosuppressive effects of ethanol (EtOH) ingestion and smoke exposure remain ill defined. To study these effects, we used a rat model that mimics chronic alcohol abuse and smoking. Rats were exposed to smoke generated by 30 reference cigarettes for one hour twice daily for 12 weeks or to room air (sham-exposed). During the last five weeks of exposure, the rats were pair-fed equal volumes of liquid diet containing 0% or 36% EtOH calories. Nasopharyngeal colonization was unaltered by EtOH ingestion and/or smoke exposure. The movement of pneumococci from the rats’ nasopharynx into the lungs was slightly increased by EtOH ingestion, but EtOH did not impair ciliary beating. Smoke exposure reduced pneumococcal movement into the lungs regardless of diet, and this was correlated with a significant increase in ciliary beat frequency. The effect of concurrent smoke exposure and EtOH ingestion on non-neutrophil (PMN)-mediated killing of pneumococci was investigated using an in vivo bactericidal assay. EtOH ingestion significantly decreased the percentage of pneumococci killed within the rats’ lungs. Unexpectedly, this EtOH-induced defect was counteracted by concurrent smoke exposure, even though smoke exposure alone did not increase intrapulmonary pneumococcal clearance. Quantification of the bactericidal proteins lysozyme and lactoferrin in the rats’ lungs did not explain the differences in non-PMN-mediated killing. However, EtOH-fed rats that were sham-exposed exhibited suppressed alveolar macrophage phagocytosis of pneumococci as well as diminished opsonization of the bacteria within their lungs. It is uncertain if smoke exposure increased macrophage ph…
author: Pitz, Adam
language: en_US
date published: 2008-12
date modified: 2026-07-24T01:50:57Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/230