Mycoplasma <i>arginini</i> enhances cytotoxicity of thioglycollate-elicited murine macrophages toward YAC-1 tumor cells through production of NO

Ribeiro‐Dias, Fátima; Russo, Marco; Barbuto, José Alexandre Marzagão; Nascimento, Flávia R.F.; Timenetsky, Jorge; Jancar, Sônia

doi:10.1002/jlb.65.6.808

Cited by 21 publications

(13 citation statements)

References 37 publications

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“…Several studies have documented M-mediated tumor cell cytotoxicity using in vitro studies of mouse peritoneal Ms [85][86][87][88]. In fact, this method of M investigation is often used to determine efficacy of various chemotherapeutic and biologic interventions [89,90].…”

Section: Importance Of Macrophage In Tumor Defensementioning

confidence: 99%

Intraperitoneal macrophages and tumor immunity: A review

Jackson

Evans

2000

J. Surg. Oncol.

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The macrophage (Mphi) is considered the first line of defense in immune response to foreign invaders. Increasing evidence suggests that Mphi(s) also play an important role against neoplastic cells. Mphi(s) exposed to supraphysiologic concentrations of CO(2) are suppressed. As surgeons apply newer minimally invasive techniques to oncologic therapies, it is important to evaluate the impact of these techniques on host-tumor interactions. We review the current understanding of Mphi biology with specific attention on cytotoxicity in addition to tumor immunity. Although systemic immune function is better preserved after laparoscopy than laparotomy, peritoneal Mphi(s) show reduced function after CO(2) pneumoperitoneum than exposure to air. Mphi(s) have shown cytotoxicity to syngeneic cancer cells and may play an important role in tumor surveillance. The impairment in Mphi function after CO(2) exposure may have an effect on outcome after oncologic surgery. In our understanding, Mphi(s) help destroy neoplastic cells. As CO(2) impairs Mphi activity, laparoscopy may significantly alter the host-tumor interaction.

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Section: Importance Of Macrophage In Tumor Defensementioning

confidence: 99%

Intraperitoneal macrophages and tumor immunity: A review

Jackson

Evans

2000

J. Surg. Oncol.

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“…Both reactive oxygen species and nitric oxygen pathways are related to antimicrobicidal activity (Higuchi et al ., 1990;Ribeiro-Dias et al ., 1999).…”

Section: Introductionmentioning

confidence: 99%

Age‐dependent change in reactive oxygen species and nitric oxide generation by rat alveolar macrophages*

et al. 2003

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SummaryImmunosenescence is an age-associated dysregulation of the immune function, which contributes to increased susceptibility to disease in the elderly. Alveolar macrophages (AM) are known phagocytes that generate reactive oxygen species (ROS) and nitric oxide (NO), essential mediators for host defence. We studied phagocytosis, ROS and NO production in AM obtained from young, adult and senescent rats (1-2, 9-12 and 18-24 months old, respectively) after exposure to lipopolysaccharide (LPS, 0.1-10 µ µ µ µ g mL), 12-O-tetradecanoylphorbol 13-acetate (TPA, 0.1 µ µ µ µ g mL − − − − 1 ) or LPS + TPA in culture. Phagocytosis was significantly lower in control AM from adult rats than in AM from young animals. Nevertheless, AM from adult animals pretreated with LPS exhibited higher phagocytic capacity than AM from younger animals. ROS was identified by the NBT test at single cell level and quantified by automated image analysis. When TPA was added to all three populations, AM from adult and senescent animals responded more than AM from young animals. All LPS-stimulated AM produce more NO than controls. However, NO production increased three-, four-and two-fold in young, adult and senescent animals, respectively. Our results demonstrate that AM from young, adult and senescent animals display differential responsiveness to inflammatory mediators. Therefore, aging processes markedly affect AM metabolic functions and may further compromise the lung immune defence response, increasing adverse long-term health effects.

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“…The TNF levels were determined in the supernatants of macrophage cultures by a biossay with L929 tumor cells [18,19]. Briefly, L929 cells were plated in 96-well flat-bottom microplates in a concentration of 5x10 4 cells/100 mL of complete medium and incubated for 24 h until obtaining a monolayer.…”

Section: Tnf Biossaymentioning

confidence: 99%

Insulin Inhibits LPS-Induced Signaling Pathways in Alveolar Macrophages

Martins

Ferracini²,

Ravanelli³

et al. 2008

Cell Physiol Biochem

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The systemic inflammatory response syndrome (SIRS) is triggered by lipopolysaccharide (LPS) from Gram-negative bacteria. Insulin was shown to have a protective role in SIRS related to sepsis. Lungs are particularly affected in this condition and provide a second wave of mediators/cytokines which amplifies SIRS. The aim of the present study was to investigate the effect of insulin on the signaling pathways elicited by LPS in alveolar macrophages (AMs) and its consequence in cellular response to LPS measured as production of tumor necrosis factor (TNF). To this purpose, resident AMs from male Wistar rats were obtained by lung lavage and stimulated by LPS (100 ng/mL). Insulin (1 mU/mL) was added 10 min before LPS. Activation (phosphorylation) of signaling molecules by LPS was analyzed by western blot, 30 min after LPS stimulation. TNF was measured in the AMs culture supernatants by bioassay using L-929 tumor cells. Relative to controls, LPS induced a significant increase in the activation of ERK (3.6-fold), p38 (4.4-fold), Tyr-326 Akt (4.7-fold), Ser-473 Akt (6.9-fold), PKCα (4.7-fold) and PKCδ (2.3-fold). Treatment of AMs with insulin before LPS stimulation, significantly reduced the activation of ERK (54%), p38 (48%), Tyr-326 Akt (64%), Ser-473 Akt (41%), PKCα (62%) and PKCδ (39%). LPS induced TNF production in AMs which was also inhibited by insulin (60%). These results show that insulin down-regulates MAPK, PI3K and PKCs and inhibits a downstream effect of LPS, TNF production, in rat AMs stimulated with LPS and suggest that the protective effect of insulin in sepsis could be through modulation of signal transduction pathways elicited by LPS in lung macrophages.

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Mycoplasma arginini enhances cytotoxicity of thioglycollate-elicited murine macrophages toward YAC-1 tumor cells through production of NO

Cited by 21 publications

References 37 publications

Intraperitoneal macrophages and tumor immunity: A review

Intraperitoneal macrophages and tumor immunity: A review

Age‐dependent change in reactive oxygen species and nitric oxide generation by rat alveolar macrophages*

Insulin Inhibits LPS-Induced Signaling Pathways in Alveolar Macrophages

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