Effect of smoking on the lipid composition of lung lining fluid and relationship between immunostimulatory lipids, inflammatory cells and foamy macrophages in extrinsic allergic alveolitis

Abstract

Normal lung lining fluid suppresses lymphoproliferative responses. This effect is mediated by the major phospholipid components, but minor lipid components can stimulate lymphocyte proliferation. The aim of this study was to discover whether the changes in lung lipid composition reported in patients with extrinsic allergic alveolitis (EAA) might influence the levels of lymphocytes which occur in the lungs of these patients. Since cigarette smokers are less susceptible to EAA, we also investigated the effect of smoking on the lipid composition of lung lining fluid. Lung lining fluid was sampled by bronchoalveolar lavage (BAL) from 15 patients with EAA, and 9 non-smokers and 13 smokers without lung disease. The smoking controls had increases in phosphatidylethanolamine, sphingomyelin and phosphatidylglycerol, but lower levels of cholesterol and cholesterol:total phospholipid ratios compared with the nonsmoking controls. By contrast, the patients with EAA had increases in total phospholipid and sphingomyelin; there were no smoking related decreases in cholesterol; and several patients had levels of cholesterol and cholesterol:total phospholipid ratios above the upper limit for the controls. In the BAL fluids of the EAA patients, the levels.ml-1 of the immunostimulatory lipids sphingomyelin, phosphatidylethanolamine, cholesterol and cholesterol esters correlated with the number.ml-1 of lymphocytes, mast cells, neutrophils and "foamy" macrophages. Cholesterol levels (rs = 0.82) and lymphocyte counts (rs = 0.90) correlated most closely with "foamy" macrophages (p less than 0.001), suggesting that uptake of cholesterol by macrophages may enhance antigen-presenting function. These observations provide some support for the hypothesis that inflammatory reactions in the lungs might be influenced by the local lipid environment.

Molecular Impact of Conventional and Electronic Cigarettes on Pulmonary Surfactant

“…The concentration of neutral lipids also appears to be increased or reduced in smokers, particularly that of cholesterol, which was detected to be decreased in past studies [96,102], conversely to what was observed in a more recent study conducted on the induced sputum supernatant [99].…”

“…The concentration of other phospholipids is also significantly dysregulated. A decrease in the concentration of phospholipids was demonstrated in smokers' BAL fluid [101] and CS was proven to alter the lipid composition of surfactant [102], inducing a selective increase in the concentrations of phosphatidylethanolamine, sphingomyelin and phosphatidylglycerol, but not of phosphatidylcholine. An increase in phosphatidylethanolamine was observed elsewhere [103].…”

Differences in BAL fluid variables in interstitial lung diseases evaluated by discriminant analysis

“…In addition, the percentage Iymphocytes is decreased. These differences in the BALF profile suggest a modification of the inflammatory reactions in the lungs, due to smoking [27].…”

The Relationship of Cholesterol Responses to Mitochondrial Dysfunction and Lung Inflammation in Chronic Obstructive Pulmonary Disease

“…A systematic lipidomic analysis of BAL fluid in subjects with COPD that had achieved smoking cessation was compared with BAL from healthy subjects, and observed a decrease in alveolar lipids, which correlated with a reduction in lung function [ 29 ]. Smoking decreases BAL fluid lipids, especially phospholipids and cholesterol, followed by sphingolipids and glycerolipids [ 32 ]. Decreases in total BAL lipid, total PL, PC 30:0, PC 32:0, and total cholesterol, amongst other lipids, strongly correlated with decreased lung function, which was also observed in the second-hand smoke mice model [ 29 ].…”