Nitric oxide modulates interleukin‐2‐induced proliferation in CTLL‐2 cells

Padrón, Julio Rodríguez; Glaria, L.; Martinez, Osvaldo; Torres, Magdalena; Lopez, E. Garcia; Delgado, René; Caveda, Luis; Rojas, Armando

doi:10.1155/s0962935196000464

Cited by 4 publications

(5 citation statements)

References 14 publications

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“…On the other hand, it has been proposed that low amounts of NO are required for optimal proliferation of T cells [3], consistent with recently discovered protective role of NO in T-cell apoptosis [23,24]. Low NO levels enhanced IL-2-induced proliferation of myelin basic protein-speci®c T-cell clone and cytotoxic T-cell line CTLL-2 [25,26], suggesting that conditions in which IL-2 is not a limiting factor can favour growth-promoting action of NO. The present report describes that an NO interference with the IL-2 action can result in an enhanced, unchanged, or reduced growth of rat lymphocytes, depending not only on NO concentration, but also on kinetics of its release.…”

Section: Discussionsupporting

confidence: 56%

Nitric Oxide Promotes Growth and Major Histocompatibility Complex‐Unrestricted Cytotoxicity of Interleukin‐2‐Activated Rat Lymphocytes

2000

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The effect of nitric oxide (NO) on growth and major histocompatibility complex(MHC)-unrestricted cytotoxicity of interleukin(IL)-2-cultivated rat spleen nonadherent mononuclear cells was examined. NO donor sodium nitroprusside (SNP) at relatively low concentrations increased magnitude, as well as duration of IL-2-induced proliferative response of nonadherent splenocytes. SNP effect depended completely on released NO, because it was prevented by NO scavenger haemoglobin, but not mimicked by expired SNP solution, unable to generate NO, or ferricyanide, a second breakdown product of SNP. Other NO donors - SIN-1, SNAP and GSNO failed to exert SNP-like growth-enhancing action, probably as a consequence of rapid NO generation, compared to sustained NO release by SNP. All NO-releasing chemicals at high concentration blocked IL-2-induced proliferation. Growth-promoting effect of SNP-derived NO was independent of guanilat cyclase activation, because dibutyryl cGMP did not affect IL-2-triggered splenocyte proliferation. Macrophage NO acted in a manner similar to SNP; at low concentrations it promoted IL-2-induced splenocyte growth, however higher amounts were suppressive. Cytotoxicity of IL-2-activated splenocytes against NK-sensitive K562 cell line was significantly increased when SNP was present during cultivation with IL-2. Proportion of NKR-P1+ and CD25+ cells, as well as per cell expression of these important activation molecules were increased upon SNP treatment, suggesting possible mechanism for the observed NO action.

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Section: Discussionsupporting

confidence: 56%

Nitric Oxide Promotes Growth and Major Histocompatibility Complex‐Unrestricted Cytotoxicity of Interleukin‐2‐Activated Rat Lymphocytes

2000

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“…CGMP indirectly activates NO synthases, and it is known that nitric oxide (NO) improves endometrial thickness by enhancing uterine blood flow (7, 9). It also improves NK activity [ 36 ]. The shortage of cGMP in the cells of RPL patients may disturb NO release and, subsequently, cause an inadequate cytotrophoblast invasion of the uterine spiral arteries and endometrium growth, as well as embryonic cell proliferation decrease [ 12 , 47 , 48 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

“…The cells were cultured at a concentration of 1 × 10 6 /mL in 4 variants: NK cells in the medium, NK cells with 400 ng/mL of sildenafil citrate (MERK, KGaA, Darmstadt, Germany), NK cells with 500 μM of NOS inhibitor—NG-Monomethyl-L-arginine, monoacetate salt (L-NMMA, (MERK, KGaA, Darmstadt, Germany), NK cells with 500 μM of L-NMMA and SC (both from MERK, KGaA, Darmstadt, Germany), [ 36 , 37 ]. The concentration of SC used in the experiments was consistent with the physiological concentration of 200 mg of orally administered Viagra in the blood of a healthy man [ 38 ].…”

Section: Methodsmentioning

confidence: 99%

Sildenafil Citrate Downregulates PDE5A mRNA Expression in Women with Recurrent Pregnancy Loss without Altering Angiogenic Factors—A Preliminary Study

Kniotek

Roszczyk

Zych

et al. 2021

JCM

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In our previous study, we showed that sildenafil citrate (SC), a selective PDE5A blocker, modulated NK cell activity in patients with recurrent pregnancy loss, which correlated with positive pregnancy outcomes. It was found that NK cells had a pivotal role in decidualization, angiogenesis, spiral artery remodeling, and the regulation of trophoblast invasion. Thus, in the current study, we determined the effects of SC on angiogenic factor expression and production, as well as idNK cell activity in the presence of nitric synthase blocker L-NMMA. Methods: NK cells (CD56+) were isolated from the peripheral blood of 15 patients and 15 fertile women on MACS columns and cultured in transformation media containing IL-15, TGF-β, and AZA—a methylation agent—for 7 days in hypoxia (94% N2, 1% O2, 5% CO2). Cultures were set up in four variants: (1) with SC, (2) without SC, (3) with NO, a synthase blocker, and (4) with SC and NO synthase blocker. NK cell activity was determined after 7 days of culturing as CD107a expression after an additional 4h of stimulation with K562 erythroleukemia cells. The expression of the PDE5A, VEGF-A, PIGF, IL-8, and RENBP genes was determined with quantitative real-time PCR (qRT-PCR) using TaqMan probes and ELISA was used to measure the concentrations of VEGF-A, PLGF, IL-8, Ang-I, Ang-II, IFN–γ proteins in culture supernatants after SC supplementation. Results: SC downregulated PDE5A expression and had no effect on other studied angiogenic factors. VEGF-A expression was increased in RPL patients compared with fertile women. Similarly, VEGF production was enhanced in RPL patients’ supernatants and SC increased the concentration of PIGF in culture supernatants. SC did not affect the expression or concentration of other studied factors, nor idNK cell activity, regardless of NO synthase blockade.

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“…Cells were plated at 10 6 cells ml −1 and incubated, for 24 h at 37°C under 5% CO 2 , with γIFN (1 μU ml −1 ) in the presence of Nm derived proteoliposome. The Griess reaction [14] was used to quantify nitrites as an index of NO production.…”

Section: Methodsmentioning

confidence: 99%

Nitric oxide participates in the immune response againstNeisseria meningitidisserogroup B

Padrón

Bebelagua

Lastre

et al. 1999

FEMS Immunology &Amp; Medical Microbiology

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The present report explores the role of nitric oxide into the immune response against Neisseria meningitidis serogroup B. Here we show that NO mediates the alphaTNF increase induced by N. meningitidis derived lipopolysaccharides (LPS), at the same time that participates in the bactericidal activity of resting or gammaIFN activated macrophages and plays a role in the specific DTH and IgG response induced by a commercial anti-meningococcal vaccine. Our findings suggest a positive role for NO at the final effector mechanisms and in the early events driving the immunity against N. meningitidis, suggesting also an insight into its role in endotoxic shock.

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Nitric oxide modulates interleukin‐2‐induced proliferation in CTLL‐2 cells

Cited by 4 publications

References 14 publications

Nitric Oxide Promotes Growth and Major Histocompatibility Complex‐Unrestricted Cytotoxicity of Interleukin‐2‐Activated Rat Lymphocytes

Nitric Oxide Promotes Growth and Major Histocompatibility Complex‐Unrestricted Cytotoxicity of Interleukin‐2‐Activated Rat Lymphocytes

Sildenafil Citrate Downregulates PDE5A mRNA Expression in Women with Recurrent Pregnancy Loss without Altering Angiogenic Factors—A Preliminary Study

Nitric oxide participates in the immune response againstNeisseria meningitidisserogroup B

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