Ory and immune processes in the lower respiratory tract which is
Ory and immune processes in the lower respiratory tract which is able to give us a deeper understanding of pathophysiologic changes brought by smoking. Typically smokers have a decrease of CD4+/CD8+ caused by higher percentage of CD8+ T-cells in BAL as compared with nonsmokers [29]. The same change of T-lymphocyte subsets was also demonstrated in the lung tissue of healthy smokers, but was in contrast with the result detected in induced sputum of PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27735993 smokers that decreased proportion of CD8+T lymphocytes with increased ratio of CD4+/CD8+ T-cells. One explanation would be the inflammatory microenvironment in airway lumen sampled by induced sputum is different from that in theZhou et al. Tobacco Induced Diseases (2016) 14:Page 3 ofBAL and airway epithelium sampled by bronchial biopsies [30]. Another reason would be smoking induced suppression of the trans-epithelial migration of CD8+ lymphocytes, increasing their number in the large airway wall, while reducing their number in the airway lumen [31]. Besides, among the subsets of CD8+T-lymphocytes, Yu et al. [32] showed a significant trend for greater Tc1/Tc2 ratio in BAL of patients with COPD and smokers compared with nonsmokers. CD8+T-lymphocytes who are key inflammatory effector and regulatory cells have been proved to play an important role in the inflammatory process of COPD [33]. CD8+T-lymphocytes can be differentiated into cells that synthesize interferon-gamma (IFN-) but not interleukin-4 (IL-4) (Tc1 cells) or cells that synthesize IL-4 but not IFN- (Tc2 cells) [34]. However, little is known about which subpopulation is mostly involved in the immuno-pathogenesis of COPD. The imbalance of the two phenotypes was actually detected in the BAL of smokers and patients with COPD. Kuschner with his co-workers [35] observed greater concentrations of monocyte chemoattractant protein (MCP)-1 with increased level of IL-6, IL-8 and IL-1 in BAL of control smokers as compared with nonsmokers, moreover, the level of IL-8 and IL-1 were elevated in a cigarette dose-dependent manner. Clara cell 10 kDa protein (CC10), which may have a role in protecting the respiratory tract from oxidative stress and inflammation by inhibiting the expression and/or activity of proteins, such as phospholipase A2, IFN-, and TNF-a was found to be significantly decreased in BAL fluids of healthy smokers in comparison with nonsmokers [36, 37]. Hence, a decrease of CC10levels in the peripheral airways as a result of smoking may be associated with enhanced pro-inflammatory process in the peripheral airways of the smokers. Molecules mediating tissue damage as matrix metalloproteinase (MMP)-9 and MMP-12 had either increased levels and/or enhanced activities in samples from BAL of smokers as compared with nonsmokers [38, 39]. CEP-37440 chemical information Surfactant protein A and D (SP-A, SP-D), members of the collectin family which play a key role in innate immunity in animal models [40], were decreased in BAL of healthy smokers vs. non-smokers [41]. Therefore, lower levels of SP-D caused by cigarette smoking may weaken lung immunity in healthy smokers. Alveolar macrophages (AM) are responsible for a broad set of host defense functions including recognition and phagocytosis of pathogenic material and apoptotic cells. Various changes of smokers’ alveolar macrophages have been noted in several studies. The number and proportion of AM in healthy smokers’ BAL are increased as compared with nonsmokers [42, 43]. And AM from smokers differ from those of nonsmokers in.
