Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms

Psychoneuroendocrinology. 1998 Feb;23(2):189-204. doi: 10.1016/s0306-4530(97)00076-0.

Abstract

Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation. This ability of nicotine to attenuate an inflammatory response may also be the cause of reduced mortality of chronically nicotine-treated mice from acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti-SRBC AFC responses were also observed after intracerebroventricular (i.c.v.) administration of relatively small concentrations of NT (28 micrograms/day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protein tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+]i. These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Abscess / drug therapy
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Body Temperature / drug effects
  • Calcium / metabolism
  • Hemolytic Plaque Technique
  • Immune System / drug effects*
  • Immunity / drug effects*
  • Influenza A virus
  • Injections, Intraventricular
  • Male
  • Mice
  • Motor Activity / drug effects
  • Nicotine / administration & dosage
  • Nicotine / pharmacology*
  • Nicotinic Agonists / administration & dosage
  • Nicotinic Agonists / pharmacology*
  • Orthomyxoviridae Infections / metabolism
  • Orthomyxoviridae Infections / physiopathology
  • Protein-Tyrosine Kinases / metabolism
  • Rats
  • Rats, Inbred Lew
  • T-Lymphocytes / drug effects
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Nicotinic Agonists
  • Nicotine
  • Protein-Tyrosine Kinases
  • Calcium