Pulmonary cytokine composition differs in the setting of alcohol use disorders and cigarette smoking. Am J Physiol Lung Cell Mol Physiol 2013 Jun 15;304(12):L873-82
Date
04/23/2013Pubmed ID
23605000Pubmed Central ID
PMC3680749DOI
10.1152/ajplung.00385.2012Scopus ID
2-s2.0-84879143691 (requires institutional sign-in at Scopus site) 25 CitationsAbstract
Alcohol use disorders (AUDs), including alcohol abuse and dependence, and cigarette smoking are widely acknowledged and common risk factors for pneumococcal pneumonia. Reasons for these associations are likely complex but may involve an imbalance in pro- and anti-inflammatory cytokines within the lung. Delineating the specific effects of alcohol, smoking, and their combination on pulmonary cytokines may help unravel mechanisms that predispose these individuals to pneumococcal pneumonia. We hypothesized that the combination of AUD and cigarette smoking would be associated with increased bronchoalveolar lavage (BAL) proinflammatory cytokines and diminished anti-inflammatory cytokines, compared with either AUDs or cigarette smoking alone. Acellular BAL fluid was obtained from 20 subjects with AUDs, who were identified using a validated questionnaire, and 19 control subjects, matched on the basis of age, sex, and smoking history. Half were current cigarette smokers; baseline pulmonary function tests and chest radiographs were normal. A positive relationship between regulated and normal T cell expressed and secreted (RANTES) with increasing severity of alcohol dependence was observed, independent of cigarette smoking (P = 0.0001). Cigarette smoking duration was associated with higher IL-1β (P = 0.0009) but lower VEGF (P = 0.0007); cigarette smoking intensity was characterized by higher IL-1β and lower VEGF and diminished IL-12 (P = 0.0004). No synergistic effects of AUDs and cigarette smoking were observed. Collectively, our work suggests that AUDs and cigarette smoking each contribute to a proinflammatory pulmonary milieu in human subjects through independent effects on BAL RANTES and IL-1β. Furthermore, cigarette smoking additionally influences BAL IL-12 and VEGF that may be relevant to the pulmonary immune response.
Author List
Burnham EL, Kovacs EJ, Davis CSAuthor
Christopher Stephen Davis MD, MPH Associate Professor in the Surgery department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AdultAge Factors
Alcoholism
Bronchoalveolar Lavage Fluid
Chemokine CCL5
Ethanol
Female
Gene Expression Regulation
Humans
Interleukin-12
Interleukin-1beta
Lung
Male
Middle Aged
Respiratory Function Tests
Risk Factors
Sex Factors
Smoking
T-Lymphocytes
Vascular Endothelial Growth Factor A
