Proposed Mechanism. It is widely accepted that cigarette smoke contributes to the development of a number of autoimmune diseases. Research over the years has shown the pro- inflammatory effects of cigarette smoke mostly in the context of emphysema and cardiovascular disease (Xxxxxxx and Xxxxx 2004). It has been demonstrated that cigarette smoke both increases total peripheral blood leukocyte counts (Xxxxx and Xxxxxxx 2001) as well as increases their export of tissue-damaging matrix metalloproteinases (Xxxxxx, Xxxxxx et al. 2001). Cigarette smoking has also been observed to be associated with significant increases in IL-6 and C-reactive protein, which both serve as markers of inflammation (Xxxxx, Psaty et al. 1997). It has also been observed that there exists a long- lasting immunosuppressive effect from cigarette smoke on T-cell-dependent autoimmune responses. After the suppressive effect has stopped, however, autoantibodies return to xxxxxx-elevated levels (Xxxxx, Xxxxxxxxx et al. 2005). A 2004 paper by Xxxxxx Xxxxxx suggests a potential mechanism for the role that cigarette smoke plays in disease activity, specifically for SLE patients. She suggests that tobacco smoke activates macrophages in the alveoli, which thereby increases free radical production as well as myeloperoxidase activity. Xxxxxx goes on to propose that long-term exposure to cigarette smoke may decrease the general activity of natural killer cells as well as disrupt the secretion of proinflammatory cytokines. Such mechanisms may add to an overall immunosuppressive effect of smoking and therefore may result in a greater vulnerability to infections. Although little information currently exists regarding the effects of tobacco smoke on the development of autoimmune diseases in general, recent research suggests that a history of smoking is associated with the prevalence of antinuclear antibodies and rheumatoid factors (Xxxxxx and Parks 2004). In addition, other research has shown support that cigarette smoke may lead to the up-regulation of genes coding for Fas (CD5), (binding receptors that induce apoptosis) on lymphocyte cell surfaces. This increase in sensitivity of white blood cells to apoptotic signals could add to the amount of apoptotic material that is needed to be cleared. Patients at risk for SLE, who already have an inefficient clearance mechanism, could therefore be more at risk for autoimmunity (Xxxxxxxxxxx and Xxxxxxx 2005). Cigarette smoking and SLE meta-analysis While evidence currently exists th...
Proposed Mechanism. 1. This MOU shall recognise that all matters or issues concerning sea turtles conservation and protection shall be subjected to the existing national laws and regulations of each Party.
Proposed Mechanism
