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home:special:smoking [11.12.2011]
paulalbert [Smoking tobacco]
home:special:smoking [10.26.2018]
sallieq [Alternatives to smoking]
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 Compounds in cigarettes have been said to be carcinogenic. As discussed in [[home:​publications:​proal_autoimmunity_2010|Amy Proal'​s presentation at the 2010 International Congress on Autoimmunity]],​ Sapkota //et al.// identified fifteen different classes of bacteria and a broad range of pathogenic organisms in five commonly smoked cigarettes tested.(({{pubmed>​long:​20064769}})) That said, the underlying disease process by which smoking is said to cause death is not well-defined. Compounds in cigarettes have been said to be carcinogenic. As discussed in [[home:​publications:​proal_autoimmunity_2010|Amy Proal'​s presentation at the 2010 International Congress on Autoimmunity]],​ Sapkota //et al.// identified fifteen different classes of bacteria and a broad range of pathogenic organisms in five commonly smoked cigarettes tested.(({{pubmed>​long:​20064769}})) That said, the underlying disease process by which smoking is said to cause death is not well-defined.
-===== Smoking and prolonged stress decrease production of antimicrobial peptides ===== 
  
-Smoking and prolonged stress have been linked to increased susceptibility to bacterial infection. A 2010 study appearing in //Cell Host and Microbe// shows that this may be caused by a decrease in antimicrobial peptide (AmP) activity as a result of increased stimulation of a neuroendocrine signalling pathway.(({{pubmed>​long:​20413096}})) Radek //et al.// showed that when nicotinic acetylcholine receptors (nAChRs) were stimulated, mice had decreased AmP production and were increasingly susceptible to the pathogens methicillin-resistant //​Staphylococcus aureus// and Group A //​Streptococcus//​ infections. 
  
  
-===== Nicotine interferes with apoptosis ​=====+===== Smoking is immunosuppressive ​===== 
 + 
 +  * **Smoking and prolonged stress decrease production of antimicrobial peptides** – Smoking and prolonged stress have been linked to increased susceptibility to bacterial infection. A 2010 study appearing in //Cell Host and Microbe// shows that this may be caused by a decrease in antimicrobial peptide (AmP) activity as a result of increased stimulation of a neuroendocrine signalling pathway.(({{pubmed>​long:​20413096}})) Radek //et al.// showed that when nicotinic acetylcholine receptors (nAChRs) were stimulated, mice had decreased AmP production and were increasingly susceptible to the pathogens methicillin-resistant //​Staphylococcus aureus// and Group A //​Streptococcus//​ infections. 
 +  * **Nicotine interferes with apoptosis** – According to a 2007 review, nicotine acts on immune cells. Although nicotine itself is usually not referred to as a carcinogen, there is ongoing debate whether nicotine functions as a "tumor enhancer."​ By binding to nicotinic acetylcholine receptors, nicotine deregulates essential biological processes like angiogenesis,​ apoptosis, and cell-mediated immunity.(({{pubmed>​long:​17846896}})) Delayed apoptosis – that is, the inability of cells to self-destruct – is one of the hallmarks of chronic inflammatory disease. It is well-documented that microbes induce delayed apoptosis in order to gain a survival advantage. 
 + 
  
-According to a 2007 review, nicotine acts on immune cells. Although nicotine itself is usually not referred to as a carcinogen, there is ongoing debate whether nicotine functions as a "tumor enhancer."​ By binding to nicotinic acetylcholine receptors, nicotine deregulates essential biological processes like angiogenesis,​ apoptosis, and cell-mediated immunity.(({{pubmed>​long:​17846896}})) Delayed apoptosis – that is, the inability of cells to self-destruct – is one of the hallmarks of chronic inflammatory disease. It is well-documented that microbes induce delayed apoptosis in order to gain a survival advantage. 
  
  
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 +{{tag>​Special_issues special }}
 ===== Notes and comments ===== ===== Notes and comments =====
  
home/special/smoking.txt · Last modified: 10.26.2018 by sallieq
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