TY  - JOUR
  - Aherne, SA, O'Brien, NM
  - 2008
  - June
  - Molecular Nutrition ; Food Research
  - Modulation of Cytokine Production By Plant Sterols In Stimulated Human Jurkat T Cells
  - Validated
  - ()
  - 52
  - 6
  - 664
  - 673
  - The plant sterols campesterol, beta-sitosterol and beta-sitostanol were investigated for potential immunomodulatory effects in Jurkat T cells. Treatments involved supplementing cells with or without concanavalin A (ConA) or phorbol-12-myristate-13-acetate plus ionomycin (PMA+IoM) in the presence or absence of increasing concentrations (10-100 mu M) of each plant sterol for 24 It. None of the plant sterols significantly affected mitogen-stimulated IL-4, IL-10 or IFN-gamma production. However, campesterol, beta-sitosterol and beta-sitostanol significantly suppressed mitogen-induced IL-2 production in a dose-dependent mariner. Both bisindolylmaleimide-I (BIM-I), a specific protein kinase C (PKC) inhibitor, and the immunosuppressant drug known as Tacrolimus (FK506), an IL-2 inhibitor, prevented mitogen-stimulated IL-2 production in Jurkat cells. Treatment with PMA+IoM alone significantly increased PKC activity and the presence of BIM-I prevented PKC activation by PMA+IoM. Following 24 It treatments, the plant sterols did not affect PMA+IoM-enhanced PKC activity, cellular calcium content or calcineurin activity. Intracellular cyclic 3',5'-adenosine monophosphate (cAMP) levels were significantly reduced by PMA+IoM. The presence of FK506 prevented a PMA+IoM-induced reduction of intracellular cAMP. Likewise the plant sterols behaved in a similar manner as FK506. Our findings suggest that the suppression of IL-2 by the plant sterols was not mediated via PKC inhibition and that their effects occurred possibly via cAMP modulation and/or a calcium/calcineurin-independent pathway..
  - DOI 10.1002/mnfr.200700385
DA  - 2008/06
ER  - 

@article{V723566,
   = {Aherne,  SA and  O'Brien,  NM },
   = {2008},
   = {June},
   = {Molecular Nutrition ; Food Research},
   = {Modulation of Cytokine Production By Plant Sterols In Stimulated Human Jurkat T Cells},
   = {Validated},
   = {()},
   = {52},
   = {6},
  pages = {664--673},
   = {{The plant sterols campesterol, beta-sitosterol and beta-sitostanol were investigated for potential immunomodulatory effects in Jurkat T cells. Treatments involved supplementing cells with or without concanavalin A (ConA) or phorbol-12-myristate-13-acetate plus ionomycin (PMA+IoM) in the presence or absence of increasing concentrations (10-100 mu M) of each plant sterol for 24 It. None of the plant sterols significantly affected mitogen-stimulated IL-4, IL-10 or IFN-gamma production. However, campesterol, beta-sitosterol and beta-sitostanol significantly suppressed mitogen-induced IL-2 production in a dose-dependent mariner. Both bisindolylmaleimide-I (BIM-I), a specific protein kinase C (PKC) inhibitor, and the immunosuppressant drug known as Tacrolimus (FK506), an IL-2 inhibitor, prevented mitogen-stimulated IL-2 production in Jurkat cells. Treatment with PMA+IoM alone significantly increased PKC activity and the presence of BIM-I prevented PKC activation by PMA+IoM. Following 24 It treatments, the plant sterols did not affect PMA+IoM-enhanced PKC activity, cellular calcium content or calcineurin activity. Intracellular cyclic 3',5'-adenosine monophosphate (cAMP) levels were significantly reduced by PMA+IoM. The presence of FK506 prevented a PMA+IoM-induced reduction of intracellular cAMP. Likewise the plant sterols behaved in a similar manner as FK506. Our findings suggest that the suppression of IL-2 by the plant sterols was not mediated via PKC inhibition and that their effects occurred possibly via cAMP modulation and/or a calcium/calcineurin-independent pathway..}},
   = {DOI 10.1002/mnfr.200700385},
  source = {IRIS}
}