The response of human bone marrow to chronic cigarette smoking

Abstract

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 ageand sex-matched nonsmoking controls.The total white cell (6.8 0.3310 9 versus 5.3 0.2310 9 cells . L -1 , p<0.0001) and PMNL (4.2 0.18310 9 versus 3.2 0.1310 9 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 0.04310 9 versus 0.03 0.001310 9 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. Eur Respir J 2000; 15: 915±921.

Relation of smoking status to a panel of inflammatory markers: The Framingham offspring

“…Whereas some investigators have shown that there is increased MPO activity in polymorphonuclear leukocytes in smokers (measured by flow cytometry), others have demonstrated no increased peroxidase activity (quantified by the MPXI, a parameter produced by automated blood counters) in neutrophils of smokers as compared with non-smokers. 32,33 We conclude that current evidence is controversial, and our finding that there was no significant elevation in serum in smokers may reflect the distinction between circulating versus tissue concentrations or may reflect differences in MPO assays.…”

Smoking and Air Pollution as Pro-Inflammatory Triggers for the Development of Rheumatoid Arthritis

“…Smoking also causes a chronic, low-grade leukocytosis characterised by increased numbers of immature neutrophils with a pro-inflammatory phenotype which accumulate in the lungs [54]. Migration of circulating neutrophils and monocytes to the lungs is facilitated by smoke-mediated: i) activation of the β2-integrin, CR3, on phagocytes together with upregulated expression of its counterreceptor ,ICAM-1, on vascular endothelium; and ii) increased production of neutrophil/monocyte-attracting chemokines, as well as endothelium-interactive, proadhesive cytokines, by smoke-exposed resident airway and infiltrating cells [55,56].…”

Harmful Interactions of Non-Essential Heavy Metals with Cells of the Innate Immune System

“…More recently, Di Lorenzo et al (2006) reported an association between Pb exposure and the numbers of circulating neutrophils, with the strongest association being observed in occupationally-exposed workers who smoked [49]. This latter observation is not surprising given the well-recognized association of smoking with: i) neutrophilia [50]; and ii) increased levels of Pb in the blood of smokers as described above. Although the authors speculate that increased numbers of circulating neutrophils may represent a mechanism to compensate for Pb-mediated immune dysfunction, they concede that it is more likely to reflect a neuroendocrine response to toxicity/stress.…”