The 2016 article concerns cigarette smoking, its potential numerous connections with disease and its impact in the current international healthcare system. The researchers state smoking impacts adaptive and innate immunity, playing a dual role in regulation of immunity via attenuation of defensive immunity or pathogenic immune responses. The types of adaptive...
The 2016 article concerns cigarette smoking, its potential numerous connections with disease and its impact in the current international healthcare system. The researchers state smoking impacts adaptive and innate immunity, playing a dual role in regulation of immunity via attenuation of defensive immunity or pathogenic immune responses. The types of adaptive immune cells that feel the impact from cigarette smoking are "T helper cells (Th1/Th2/Th17), CD4+CD25+ regulatory T.
cells, CD8+ T cells, B cells and memory T/B lymphocytes while innate immune cells impacted by smoking are mostly DCs, macrophages and NK cells" (Qiu et al., 2015, p. 1). The changes in these cells due to smoking can lead to numerous chronic or acute diseases like autoimmune diseases, cancers and transplant rejection, respiratory and cardiovascular diseases, and allergies. The researchers note past studies connect smoking with specific diseases such as lung cancer and emphysema, however not enough updated reviews are performed to see smoking's impact on general immunity.
Furthermore, little research exists on smoking's impact on major components of immune cells. The aim of article is to objective and systematically review cigarette smoking's influence on significant components of adaptive and innate immune cells, as well as summarize molecular and cellular mechanisms that underlie the effects on the immune system from cigarette smoking. They found the molecular pathways cigarette smoking impacts involve histone modification and MAP, NFkB kinases. They end with a concluding statement suggesting further examination on the true impact cigarette smoking has regarding smoking-mediate immunopathology.
Because, even though smoking has a dual effect on a person's immune responses, the overall effect is negative. Therefore, more investigation on the specific negative impact may produce a distinct causal link to some diseases that exist today like multiple sclerosis or any other immune related illness. Although the paper does a good job of explaining the potential cause of some diseases due to cigarette smoking, there is no finite link to anything.
This is odd considering so much research has been performed on cigarette smoking and its adverse health effects. The aspect that was important and added to the legitimacy of the review is describing the number of people that smoke tobacco. At roughly 1/3 of the world population, cigarette smokers are numerous. By detailing what is in a cigarette like nicotine and cadmium, the picture of a dangerous substance was made clear. This was well executed within the first paragraph of the introduction.
Going back to specificity, there was no mention of a clear cause of disease, rather an effect of cigarette smoking on allograft survival via costimulatory blockade. Table 1, which was meant to show which diseases are caused by cigarette smoking only provide the names, they do not show the reasons why cigarette smoking causes them. This is where the review lacks breadth and depth.
If the point of the article is to show the general impact on immunity, why not show the potential impact in these specific illnesses like lupus or rheumatoid arthritis? This was the main problem with the article. From this, the article goes haphazardly into the effects of cigarette smoking on adaptive immunity. T lymphocytes, T helper cells, are discussed and shown to increase or decrease in circulation in patients with COPD.
The researchers made an epidemiological correlation with cigarette smoking and Crohn's disease based on prior research and state the possible effect smoking has on TH17 and TH1 cells can be the reason why it plays a role in development of Crohn's disease. Specifically, they noted the nicotine in cigarettes can have an impact on TH17 production. But the evidence is not clear, demonstrating contradictory evidence. "The contradictory effects of smoke/nicotine on two types of experimental colitis in mice resulted from different pathologic changes.
It has been known that TNBS-induced colitis was Th1 cell-mediated whereas oxazolone-induced colitis was Th2 cell-oriented" (Qiu et al., 2015, p. 3). This kind of contradictory, never implicit connections continues with CD8 and T. cells where although there is mention of many studies showing smoking increasing the quantity of T. cells and CD8, there is also contradictory information illustrating a reduction in these cells and no specific tie into how cigarettes directly impact health and cause of disease.
Although they mention the dual effects of cigarette smoking on immunity in the introduction, they need to also demonstrate specificity and certainty in some regard to the negative aspects of smoking on immunity. They try to do this by explaining the role of regulatory T. cell (Treg). Tregs plays a vital role in immunological homeostasis maintenance and tolerance.
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