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Cigarette Smoke Inhibits Human Bronchial Epithelial Cell Repair Processes

By interfering with the ability of airway epithelial cells to support repair processes, cigarette smoke could contribute to alterations of airway structures and functions that characterize chronic obstructive pulmonary disease (COPD). The current study assessed the ability of cigarette smoke extract (CSE) to alter human airway epithelial cell chemotaxis, proliferation, and contraction of three-dimensional collagen gels, a model of extracellular matrix remodeling. The volatile components contained in cigarette smoke, acetaldehyde and acrolein, were able to inhibit all three processes. Nonvolatile components contained within lyophilized CSE also inhibited chemotaxis but displayed no activity in the other two bioassays. CSE also inhibited the ability of airway epithelial cells to release transforming growth factor (TGF)- β and fibronectin. Exogenous fibronectin was unable to restore epithelial cell contraction of collagen gels. Exogenous TGF- β partially restored the ability of airway epithelial cells to contract collagen gels and to produce fibronectin. This supports a role for inhibition of TGF- β release in mediating the inhibitory effects of cigarette smoke. Taken together, the results of the current study suggest that epithelial cells present in the airways of smokers may be altered in their ability to support repair responses, which may contribute to architectural disruptions present in the airways in COPD associated with cigarette smoking.

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Effect of Molybdenum-Induced Copper Deficiency on In Vivo and In Vitro Measures of Neutrophil Chemotaxis both Before and Following an Inflammatory Stressor

Twelve Angus Hereford heifers (avg wt=183.6kg) were allotted by initial liver copper (Cu) concentrations into one of two treatments. Control (n=6) heifers were fed a basal diet supplemented to provide a dietary Cu level of 10ppm. Molybdenum (Mo)-induced Cu-deficient heifers (n=6) were fed an identical basal diet supplemented with sodium molybdate (Cu:Mo ratio = 1:2.5), with dietary sulfur at .3% of the total diet. Dietary treatments were delivered for 120d, at which time Mo-supplemented heifers were considered Cu-deficient (286 and 49ppm liver Cu for control and Mo-induced Cu-deficient, respectively). Peripheral blood neutrophils were enumerated both before and after the administration of an inflammatory stressor, a subcutaneous injection (1.5mL) of Freund’s complete adjuvant. In vitro and in vivo measures of neutrophil chemotaxis were evaluated and the expression of two adhesion molecules, CD18 and L-selectin, were analyzed by flow cytometric procedures. Molybdenum-induced Cu deficiency increased (P<.01) the number of peripheral blood neutrophils; however, in vitro neutrophil chemotaxis was not affected. In vivo neutrophil chemotaxis tended (P<.08) to be increased in Mo-induced Cu-deficient heifers (1.55 vs 2.26 x 106 cells/sponge for control and Mo-supplemented, respectively). No differences in CD18 or L-selectin expression were detected between treatments. However, CD18 expression was decreased (P<.05) in both treatments following adjuvant injection. These data suggest that Mo-induced Cu deficiency results in an increase in peripheral blood neutrophil number, without altering chemotactic ability and adhesion molecule expression.

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