It is proved that smoking invokes serious diseases, such as emphysema and cancer. However, a new study shows that the stimulation of nicotinic receptors in the cells of the immune system may become the treatment of inflammatory lung diseases.
"In tests with animals stimulation of PNU-282987 alpha-7 nicotinic receptor experimental drug reduces inflammation in allergic condition like asthma, and in a model of lung inflammation," - says Camila Prado, chief researcher of the Federal University of São Paulo (Brazil ).
In this case, the therapeutic effect is associated with the activation of the nicotinic alpha-7 receptor in macrophages, immune system cells that are fundamental in response to a potential threat. Tests have shown that in mice with inflammation improves the condition of the lungs in the treatment of the drug due to the larger number of reducing tissue macrophages.
Nicotinic receptors are a part of the nervous system, which is the main neurotransmitter acetylcholine. However, in a previous study conducted in collaboration with scientists from the University of Western Ontario, Canada, scientists have noted that in mice with suppressed acetylcholine observed exacerbation of inflammatory response in the lungs, even without any diseases or allergies. Studies show that acetylcholine has a protective effect on the lungs, which is associated with the activation of nicotinic receptors.
The level of acetylcholine in mice was 75 percent lower, as a result they have observed inflammation of the airways, similar to that seen in people with asthma. Furthermore, cell signaling pathways have been modified associated with pulmonary inflammatory response.
Based on these findings, the researchers decided to test the hypothesis that stimulation of a drug that binds to nicotinic receptors may ease inflammation in the lungs of mice.
The first tests were performed using classical mouse model of acute lung injury. The researchers injected the animals the bacterial toxin.
"About 30 minutes before injection of some mice were treated with drug PNU-282987, which stimulates nicotinic receptors alpha-7. Another group was treated with the same compound in six hours after injection, when inflammation has reached its peak. In both cases, we observed a significant reduction in inflammation compared to the control group of mice - Prado said - We assessed the effect of the drug on lung macrophages:. there was a higher proportion of M2 macrophages, which are responsible for the recovery of damaged tissue ".
lung tissue analysis showed that the treatment decreased the activation of protein NF-kB, which stimulates the production of inflammatory molecules. According to Prado said the treatment had a positive effect on the model of chronic inflammation.