Effect of ouabain on lymphokine-activated killer cells

Olej, Beni; Rocque, Lucia de La; Castilho, F.P.D.; Mediano, Isabella F.; Campos, Maria Martha; Rumjanek, Vivian M.

doi:10.1016/0192-0561(94)90097-3

Cited by 13 publications

(12 citation statements)

References 15 publications

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“…If this is true, it could be a mechanism involved in GLPinduced TNF-␣ secretion. In the PBMC, Na,K-ATPase inhibition induces proinflammatory cytokine secretion by monocytes and abolishes lymphocyte proliferation, with no influence on its early activation (7,27,30,31). Foey and coworkers (16) showed that blocking mononuclear cell Na,KATPase with ouabain induced TNF-␣ and IL-1 secretion.…”

Section: Vol 70 2002 L Interrogans Glycolipoprotein and Cellular Amentioning

confidence: 99%

Peripheral Blood Mononuclear Cell Activation Induced byLeptospira interrogansGlycolipoprotein

et al. 2002

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Section: Vol 70 2002 L Interrogans Glycolipoprotein and Cellular Amentioning

confidence: 99%

Peripheral Blood Mononuclear Cell Activation Induced byLeptospira interrogansGlycolipoprotein

et al. 2002

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“…Since then, a number of workers, including ourselves, has described the inhibitory effects of ouabain on lymphocyte proliferation induced by various stimuli such as mitogens (Szamel et al 1981, Moraes et al 1989, Olej et al 1998, phorbol ester (Olej et al 1994, Brodie et al 1995, CD3 (Szamel et al 1995), Interleukin-2 (Redondo et al 1986) and calcium ionophore (Jensen et al 1977).…”

Section: Introductionmentioning

confidence: 99%

Ouabain exacerbates activation-induced cell death in human peripheral blood lymphocytes

Esteves

Marques‐Santos

Affonso-Mitidieri

et al. 2005

An. Acad. Bras. Ciênc.

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Lymphocytes activated by mitogenic lectins display changes in transmembrane potential, an elevation in the cytoplasmic Ca 2+ concentrations, proliferation and/or activation induced cell death. Low concentrations of ouabain (an inhibitor of Na + ,K + -ATPase) suppress mitogen-induced proliferation and increases cell death. To understand the mechanisms involved, a number of parameters were analyzed using fluorescent probes and flow cytometry. The addition of 100nM ouabain to cultures of peripheral blood lymphocytes activated with 5µg/ml phytohemagglutinin (PHA) did not modify the increased expression of the Fas receptor or its ligand FasL induced by the mitogen. However, treatment with ouabain potentiated apoptosis induced by an anti-Fas agonist antibody. A synergy between ouabain and PHA was also observed with regard to plasma membrane depolarization. PHA per se did not induce dissipation of mitochondrial membrane potential but when cells were also exposed to ouabain a marked depolarization could be observed, and this was a late event. It is possible that the inhibitory effect of ouabain on activated peripheral blood lymphocytes involves the potentiation of some of the steps of the apoptotic process and reflects an exacerbation of the mechanism of activation-induced cell death.

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“…Since then, a number of workers, including ourselves, have described the inhibitory effects of ouabain on lymphocyte proliferation induced by various stimuli such as mitogens [135][136][137], phorbol ester [138,139], CD3 [140], calcium ionophore [141], IL-2 [142] and to a much lesser extent IL-4 [142]. It has been reported that both CD4 and CD8 lymphocytes are equally inhibited [139].…”

Section: Effect Of Ouabain On T Lymphocyte Proliferation and Activationmentioning

confidence: 99%

Effect of Ouabain on the Immune System

Echevarria-Lima¹,

Rumjanek

2006

CHYR

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Immune dysfunction has been reported in patients with hypertension and in spontaneously hypertensive rats. Increased circulating levels of ouabain were observed in experimental models and in human hypertension. Despite the correlation between immunologic depression and hypertension, the mechanisms involved are unclear. This review examines evidences of immune dysfunction in hypertension and presents observations suggesting that ouabain is capable of inducing lymphocyte changes related to some of the immune disturbances observed. Defects in thymocytes, mature lymphocyte subsets, lymphocyte proliferation, cytokines balance and increased immunoglobulin production, were reported in animal models and/or hypertensive patients. Ouabain potentiates the effects of glucocorticoids on thymocytes, inducing plasma membrane depolarization, loss of mitochondrial membrane potential, changes in CD69 levels, increased intracellular calcium and apoptosis of thymocyte subsets. The activation of mature lymphocytes is inhibited by ouabain following different stimuli and these cells display changes in c-myc, CD69 and CD25 levels, plasma membrane polarization and mitochondrial membrane potential. These cells underwent apoptosis, suggesting an exacerbation of the process of activation induced cell death. Levels of cytokines such as IL-1, IL-2, IL-6, TNF, and GM-CSF are modified by ouabain. Some of the ouabain effects may result from a mechanism different from the traditional inhibition of the Na + /K + ATPase.

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Effect of ouabain on lymphokine-activated killer cells

Cited by 13 publications

References 15 publications

Peripheral Blood Mononuclear Cell Activation Induced byLeptospira interrogansGlycolipoprotein

Peripheral Blood Mononuclear Cell Activation Induced byLeptospira interrogansGlycolipoprotein

Ouabain exacerbates activation-induced cell death in human peripheral blood lymphocytes

Effect of Ouabain on the Immune System

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