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Immunotoxic mechanisms of cigarette smoke and heat-not-burn tobacco vapor on Jurkat T cell functions.
Scharf, Pablo; da Rocha, Gustavo H O; Sandri, Silvana; Heluany, Cintia S; Pedreira Filho, Walter R; Farsky, Sandra H P.
Afiliación
  • Scharf P; Department of Clinical & Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, SP, Brazil.
  • da Rocha GHO; Department of Clinical & Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, SP, Brazil.
  • Sandri S; Department of Clinical & Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, SP, Brazil.
  • Heluany CS; Department of Clinical & Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, SP, Brazil.
  • Pedreira Filho WR; Fundação Jorge Duprat Figueiredo de Segurança e Medicina do Trabalho, Ministério do Trabalho e Previdência Social, Sao Paulo, SP, Brazil.
  • Farsky SHP; Department of Clinical & Toxicological Analyses, School of Pharmaceutical Sciences, University of Sao Paulo, SP, Brazil. Electronic address: sfarsky@usp.br.
Environ Pollut ; 268(Pt B): 115863, 2020 Oct 21.
Artículo en Inglés | MEDLINE | ID: mdl-33126161
ABSTRACT
Cigarette smoke (CS) affects immune functions, leading to severe outcomes in smokers. Robust evidence addresses the immunotoxic effects of combustible tobacco products. As heat-not-burn tobacco products (HNBT) vaporize lower levels of combustible products, we here compared the effects of cigarette smoke (CS) and HNBT vapor on Jurkat T cells. Cells were exposed to air, conventional cigarettes or heatsticks of HNBT for 30 min and were stimulated or not with phorbol myristate acetate (PMA). Cell viability, proliferation, reactive oxygen species (ROS) production, 8-OHdG, MAP-kinases and nuclear factor κB (NFκB) activation and metallothionein expression (MTs) were assessed by flow cytometry; nitric oxide (NO) and cytokine levels were measured by Griess reaction and ELISA, respectively. Levels of metals in the exposure chambers were quantified by inductively coupled plasma mass spectrometry. MT expressions were quantified by immunohistochemistry in the lungs and liver of C57Bl/6 mice exposed to CS, HNBT or air (1 h, twice a day for five days via inhalation). While both CS and HBNT exposures increased cell death, CS led to a higher number of necrotic cells, increased the production of ROS, NO, inflammatory cytokines and MTs when compared to HNBT-exposed cells, and led to a higher expression of MTs in mice. CS released higher amounts of metals. CS and HNBT exposures decreased PMA-induced interleukin-2 (IL-2) secretion and impaired Jurkat proliferation, effects also seen in cells exposed to nicotine. Although HNBT vapor does not activate T cells as CS does, exposure to both HNBT and CS suppressed proliferation and IL-2 release, a pivotal cytokine involved with T cell proliferation and tolerance, and this effect may be related to nicotine content in both products.
Texto completo: Disponible Colección: Bases de datos internacionales Base de datos: MEDLINE Idioma: Inglés Revista: Environ Pollut Asunto de la revista: Salud Ambiental Año: 2020 Tipo del documento: Artículo País de afiliación: Brasil

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Texto completo: Disponible Colección: Bases de datos internacionales Base de datos: MEDLINE Idioma: Inglés Revista: Environ Pollut Asunto de la revista: Salud Ambiental Año: 2020 Tipo del documento: Artículo País de afiliación: Brasil
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