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Nicotine May Affect Inflammation

Institution: University of California, San Francisco
Investigator(s): Frederick Jia-Pei Miao, M.D., Ph.D.
Award Cycle: 1999 (Cycle 8) Grant #: 8RT-0032 Award: $435,425
Subject Area: Nicotine Dependence
Award Type: Research Project Awards

Initial Award Abstract
Many diseases are characterized by inflammation, i.e., redness and soreness and swelling and this inflammation causes much suffering. The process of inflammation in the body has been shown to complex and to be modified by actions of the nervous system and action of hormones. Recently, it was found in some animal studies that nicotine stimulates hormone release that then can suppress the response of the body to produce inflammation. Another pathway in the body was found that also suppresses inflammation and uses similar hormones. This pathway is activated by pain signals. This latter pathway may function in the body to prevent inflammation from becoming overly active or persistent. Both of these effects, the effect of nicotine and the effect of pain signals, are much more prominent when a certain nerve in the body, the vagus nerve, is cut. When the vagus nerve is cut, nicotine can suppress inflammation when given at extremely low levels. We hypothesize that receptors sensitive to nicotine present on the ends of nerve fibers entering the spinal cord are important in producing both these effects. We also hypothesize that the effect of the vagus nerve (which is removed by cutting it) is produced by nerve fibers that come down thespinal cord and release chemicals similar to morphine and adrenaline in the spinal cord. We also hypothesize that the same type of effects of morphine and adrenaline-like compounds affect the action of nicotine to produce inflammation when injected into tissues. In individuals who smoke all of these mechanisms would be expected to be altered and there may also be an effect in individuals exposed to second hand smoke. Understanding the mechanisms involved in these processes should provide important information for the care of patients who smoke and in particular for patients who are smokers who also have a disease in which there is usually inflammation such as arthritis, asthma, bronchitis, inflammation of the intestines or other diseases.

Endogenous opioids suppress activation of nociceptors by sub-nanomolar nicotine
Periodical: British Journal of Pharmacology Index Medicus:
Authors: Miao FJ-P, Benowitz N, Levine JD ART
Yr: 2001 Vol: 133 Nbr: Abs: Pg: 23-28

Spino-bulbo-spinal pathway mediating vagal modulation of nociceptive-neuroendocrine control of inflammation in the rat
Periodical: Journal of Physiology Index Medicus:
Authors: Miao FJ-P, Janig W, Levine JD ART
Yr: 2001 Vol: 532 Nbr: Abs: Pg: 811-822

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activation by capsaicin in the rat paw: role of the adrenal medulla
Periodical: Journal of Physiology Index Medicus:
Authors: Miao FJ-P, Janig W, Levine JD ART
Yr: 2000 Vol: 527 Nbr: Abs: Pg: 601-610

Inhibition of nociceptive neuroendocrine control of inflammation by the periaqueductal gray and interaction with the vagus-induced inhibition in rats.
Periodical: Neuroscience Index Medicus:
Authors: Miao FJ-P, Janig W, Jasmin L, Levine JD ART
Yr: 0 Vol: Nbr: Abs: Pg: