Elsevier

Cellular Immunology

Volume 192, Issue 1, 25 February 1999, Pages 48-53
Cellular Immunology

Regular Article
Effects of Cigarette Smoking on Fas/Fas Ligand Expression of Human Lymphocytes

https://doi.org/10.1006/cimm.1998.1432Get rights and content

Abstract

Cigarette smoking has been shown to affect human immune responses. We have studied Fas/Fas ligand (FasL) expression, which is involved in the cytotoxic activity, immune privilege, and self-tolerance, and other apoptosis-associated molecule expression of peripheral blood lymphocytes (PBL) in healthy subjects with/without cigarette smoking. We found that expression of FasL protein was detected marginally in the fresh PBL and was induced upon mitogen activation in normal individuals without smoking. In contrast, fresh PBL from those with chronic cigarette smoking exhibited enhanced expression of FasL protein withoutin vitromitogen stimulation. Moreover, mitogen stimulation failed to augment FasL protein expression of their lymphocytes, suggesting dysregulation of FasL expression of PBL in individuals with cigarette smoking. In contrast, Fas, Bcl-2, and p53 expression were not significantly different between normal individuals with chronic cigarette smoking and those without smoking. In addition, we found thatin vitrobrief treatment with nicotine induces and/or enhances FasL mRNA and protein expression of lymphocytes from normal donors without smoking. These results suggest that aberrant FasL expression of lymphocytes is, at least in part, involved in the immune impairment in individuals with chronic cigarette smoking.

References (40)

  • B.D. Evavold et al.

    Immunol. Today

    (1993)
  • J. Sloan-Lancaster et al.

    Curr. Opin. Biol.

    (1995)
  • S. Nagata

    Adv. Immunol.

    (1994)
  • H. Kojima et al.

    Immunity

    (1994)
  • Y. Geng et al.

    Toxicol. Appl. Pharmacol.

    (1995)
  • T. Suda et al.

    Cell

    (1993)
  • M.L. Sopori et al.

    J. Neuroimmunol.

    (1998)
  • P.G. Holt

    Thorax

    (1987)
  • J.D. Johnson et al.

    Crit. Rev. Toxicol.

    (1990)
  • M.L. Sopori et al.

    Adv. Biosci.

    (1993)
  • J. Dhein et al.

    Nature

    (1995)
  • S. Hanabuchi et al.

    Proc. Natl. Acad. Sci. USA

    (1994)
  • T. Suda et al.

    J. Immunol.

    (1995)
  • H. Arase et al.

    J. Exp. Med.

    (1995)
  • M.R. Alderson et al.

    J. Exp. Med.

    (1995)
  • D. Kabelitz et al.

    Immunol. Today

    (1993)
  • T. Brunner et al.

    Nature

    (1995)
  • S.-T. Ju et al.

    Nature

    (1995)
  • A. Anel et al.

    Eur. J. Immunol.

    (1994)
  • Cited by (58)

    • Impact of cell death pathway genes Fas 21377AA and FasL 2844CC polymorphisms on the risk of developing non-small cell lung cancer

      2018, Egyptian Journal of Medical Human Genetics
      Citation Excerpt :

      Also, Zhao et al. (2016) observed that the risk of lung cancer was increased significantly among both smokers and non-smokers with more pronounced increase among heavy smokers than light smokers [29]. Moreover, because tobacco smoking can provoke FasL expression Suzuki et al. (1999) and Bijl et al. (2001) stated another hypothesis for this relation, where the level of FasL expression from the FasL 2844C allele was higher than that from the FasL 2844T allele upon induction by smoking and in addition to the higher constitutive expression resulting from the FasL 2844T/C polymorphism, smoking and FasL 2844CC genotype increase vulnerability of lung cancer [30,31]. Zhang et al. (2005) stated that the high level of environmental smoke that non-smokers exposed to throughout ordinary life may justify the higher risk of lung cancer among non smokers carrying FasL 2844CC genotype when compared with those carrying the same genotype and smoked less than 20 packs per year [18].

    • FASL-844 T/C polymorphism: A biomarker of good prognosis of breast cancer in the Tunisian population

      2012, Human Immunology
      Citation Excerpt :

      Moreover, the effect of a single polymorphism may be modulated by interaction with environmental and genetic factors. FASL expression can be induced by tobacco smoking [30] and alcohol consumption [31]. However, Crew et al. did not find any association between FASL genotypes and breast cancer risk by smoking status and alcohol consumption among Americans [28].

    • Effects of lifestyle on micronuclei frequency in human lymphocytes in Japanese hard-metal workers

      2009, Preventive Medicine
      Citation Excerpt :

      Furthermore, smoking may induce apoptosis more than micronuclei, and the deficiency of MN in the very heavy smokers might be explained by the fact that micronucleated cells are preferentially eliminated by apoptosis (Fig. 3). In fact, some studies have shown smoking greatly decreased NK cell numbers in peripheral blood lymphocytes (Li et al., 2007), and smoking (i.e. nicotine) induces apoptosis in human lymphocytes by enhancing expression of Fas (CD95) death receptor (Suzuki et al., 1999), increases apoptotic T cells by decreasing Bcl-2 and IL-7 receptor expression (Hodge et al., 2005). Smoking also induces apoptosis in rat terminal bronchiole through the p53/Bax and JNK/FasL cascade pathway (Wu et al., 2006).

    View all citing articles on Scopus

    This work was supported in part by the 1995–1998 SRF Foundation grants for Biomedical Research (Tokyo, Japan).

    2

    To whom correspondence and reprint requests should be addressed at Departments of Immunology and Medicine, St. Marianna University School of Medicine, 2-16-1, Sugao, Miyamae-ku, Kawasaki, Kanagawa 216-8511, Japan. Fax: 81-44-975 4347.

    View full text