The response of human bone marrow to chronic cigarette smoking

• Published in: The European respiratory journal Vol. 15; no. 5; pp. 915 - 921
• Main Authors: van Eeden, SF, Hogg, JC
• Format: Journal Article
• Language: English
• Published: Sheffield Eur Respiratory Soc 01.05.2000; Munksgaard International Publishers; Maney
• Subjects: Adult; Band cells; Biological and medical sciences; Bone Marrow - physiopathology; cell adhesion molecules; Female; Humans; Immunophenotyping; l‐selectin; Male; Medical sciences; Middle Aged; myeloperoxidase; neutrophils; Neutrophils - immunology; Pneumology; polymorphonuclear leukocytes; Respiratory system : syndromes and miscellaneous diseases; Smoking - adverse effects; Smoking - blood; Tobacco, tobacco smoking; Toxicology; Human; Pathophysiology; Respiratory disease; Leukocyte; Tobacco smoking; Bronchus; Inflammation; Case control study; Experimental study; Chronic; Leukocytosis; Bone marrow; Bronchus disease; Biological effect; Polymorphism
• ISSN: 0903-1936; 1399-3003
• DOI: 10.1034/j.1399-3003.2000.15e18.x

Chronic cigarette smoking in humans causes leukocytosis. Animal studies show that chronic smoking shortens the transit time of polymorphonuclear leukocytes (PMNLs) through the bone marrow. The present study examines the response of human bone marrow to chronic cigarette smoking. Three characteristics of peripheral blood PMNLs that indicate active bone marrow release (band cell counts, surface l‐selectin expression and myeloperoxidase (MPO) content), were measured in 38 healthy chronic smokers (23±5 pack‐yrs) and 15 age‐ and sex‐matched nonsmoking controls. The total white cell (6.8±0.3×109versus 5.3±0.2×109 cells·L‐1, p<0.0001) and PMNL (4.2±0.18×109versus 3.2±0.1×109 cells·L‐1, p<0.003) counts were higher in smokers as were the percentage (4.8±0.6 versus 1.1±0.2, p<0.0001) and total number (0.21±0.04×109versus 0.03±0.001×109 cells·L‐1, p<0.01) of band cells. Flow cytometry showed that the mean fluorescence intensity (MFI) of l‐selectin (3.2±0.2 versus 2.6±0.1, p<0.05) on PMNLs was higher in smokers. There was no difference in the baseline or N‐formyl‐methionyl‐leucyl‐phenylalanine‐stimulated expression of CD63 or CD18/CD11b (surface markers of PMNL activation) between smokers and controls. The MPO content of PMNLs was higher in smokers (3.4±0.3 versus 1.7±0.2 MFI, p<0.05). Smokers with a low (<75% of the predicted value) diffusing capacity of the lung for carbon monoxide had higher PMNL MPO levels than smokers with a diffusing capacity of >75% pred (p<0.05). In conclusion, chronic smoking causes phenotypic changes in circulating polymorphonuclear leukocytes that are characteristic of chronic stimulation of the bone marrow and it is speculated that the increased number of immature polymorphonuclear leukocytes contributes to the chronic lung inflammation associated with cigarette smoking.