Acute effects of tobacco smoke on human airway dendritic cellsin vivo

Abstract

Airway dendritic cells (DCs) play a key role in smoke-related lung diseases; however, the acute effects of tobacco smoke on human airway DCs in vivo are unknown.A total of 16 smokers underwent bronchoalveolar lavage at two time-points: directly after a 4-h period of nonsmoking (no smoke exposure); and directly after a 4-h period during which eight cigarettes were smoked (acute smoke exposure). Using flow cytometry, myeloid DCs (mDCs) and plasmacytoid DCs (pDCs), as well as function-associated surface molecules on mDCs, were analysed in bronchoalveolar lavage fluid (BALF) and in blood.The numbers of macrophages, lymphocytes, neutrophils, eosinophils and pDCs were unchanged in BALF following acute smoke exposure, as compared to no smoke exposure. In contrast, there was a strong increase in mDC number in BALF and a concomitant decrease in mDC number in blood following acute smoke exposure. In addition, acute smoke exposure led to an increase in the expression of the surface molecules blood dendritic cell antigen 1 and 4 and a decrease in the expression of the lung homing receptor, CC chemokine receptor 5, on mDCs in BALF.Acute tobacco smoke inhalation results in an immediate and selective recruitment of mDCs into human airways, which might reflect the very early reaction of the adaptive immune system to smoke exposure.

Plasmacytoid dendritic cells in pulmonary lymphoid follicles of patients with COPD

“…These results are in accordance with the findings in BAL fluid after acute smoke exposure [28] and indicate that smoking as such does not influence the number of pDCs in the airways and lymphoid follicles. As immature pDCs are present in the mucosal areas of the lung, they can be directly influenced by the effects of cigarette smoke.…”

Dendritic Cells in Human Lung Disease

“…These cDC show prominent expression of the Langerhans' cell markers langerin and CD1a and the costimulatory molecules CD80 and CD86 39 . The effects of cigarette smoke on DC production of IL-8 and prostaglandin E2 appears to be mediated via both oxidative stress and the direct effects of nicotine 40 .…”

“…It is clear that cigarette smoking per se can lead to increases in the number of lung cDC, even in the absence of overt lung disease 39 . These cDC show prominent expression of the Langerhans' cell markers langerin and CD1a and the costimulatory molecules CD80 and CD86 39 .…”

Cellular Defences of the Lung: Comparative Perspectives

“…Havenith et al, 1993;Xia et al, 1995): within 12 hours, the lung derived DCs can be found in the T-cell area of draining mediastinal lymph nodes of the lung. Inflammatory diseases of the human lung are associated with the different phenotypes and the process of the recruitment of the airway DCs (Lommatzsch et al, 2007(Lommatzsch et al, , 2010Geurtsvankessel and Lambrecht, 2008;Vassallo et al, 2010). Regulation of galectin-3 in the lungs may represent one of the multiple potential mechanisms by which galectins contribute to modulation of the innate and acquired immune responses (Maldonado et al, 2011).…”

“…Highly specialized and notably heterogenous, DCs function as messengers and regulators between innate and acquired immunity (e.g. Reid, 1997;Hart, 1997;Banchereau and Steinman, 1998;Austyn, 1998;Satthaporn and Eremin, 2001;Dzionek et al, 2000;Webb et al, 2005;McKenna et al, 2005;Lommatzsch et al, 2007Lommatzsch et al, , 2010GeurtsvanKessel and Lambrecht, 2008;von Garnier and Nicod, 2009). Because DCs have the ability to induce a primary immune response in resting naïve T-lymphocytes and play a role in the maintenance of B-cell function and antigen memory (recall) responses (e.g.…”