Effects of Substance P on the Cell Proliferation and IL-2 Production of T Lymphocyte

Substance P가 T 임파구의 세포증식과 IL-2 생산에 미치는 영향

  • Moon, Jin-Kyun (Department of Periodontology, College of Dentistry, Chon-buk National University) ;
  • Choi, Byung-Son (Department of Periodontology, College of Dentistry, Chon-buk National University) ;
  • Lee, Seok-Cho (Department of Periodontology, College of Dentistry, Chon-buk National University) ;
  • Kim, Hyung-Seop (Department of Periodontology, College of Dentistry, Chon-buk National University)
  • 문진균 (전북대학교 치과대학 치주과학교실, 전북대학교 치의학 연구소) ;
  • 최병선 (전북대학교 치과대학 치주과학교실, 전북대학교 치의학 연구소) ;
  • 이석초 (전북대학교 치과대학 치주과학교실, 전북대학교 치의학 연구소) ;
  • 김형섭 (전북대학교 치과대학 치주과학교실, 전북대학교 치의학 연구소)
  • Published : 1997.12.31

Abstract

Immune responses of periodontal tissue may be regulated by products of sensory afferent nerve endings such as neuropeptides. Substance P(SP), a tachykinin neuropeptide, has been previously reported to stimulate the activities of T lymphocyte. Therefore, I examined the role of SP in IL-2 production and cell proliferation by using a homogeneous line of T lymphocytes(Jurkat and HuT78). Cell proliferation rate was determined by [$^3H$]-thymidine incorporation test, and IL-2 was quantitated by the growth rate of CD4+ IL-2-dependent T lymphocyte line CTLL-2. SP stimulated cell proliferation of T lymphocytes at the concentration of $10^{-12}$ and $10^{-8}$M in a biphasic bell-shape dose-dependent manner. However, SP alone did not induce IL-2 release at the concentration range of $10^{-6}$ to $10^{-14}$M. The upregulation of IL-2 release was observed when $10^{-12}$M SP was applied together with mitogens such as Con A or PHA+PMA on T cell lines, especially on Jurkat. Con A or PHA+PMA demonstrated to increase the rate of cell proliferation of Jurkat, which had shown to produce much amount of IL-2 indicating that mitogen-induced cell proliferation might be partially influenced by released IL-2. It was concluded that regulatory effects of SP on the immune/inflammatory response could be mediated through the costimulatory upregulation of IL-2 production and increase of cell proliferation of T lymphocyte.

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