Demonstration of iNOS-mRNA and iNOS in human monocytes stimulated with cancer cells <i>in vitro</i>

Siedlar, Maciej; Mytar, B; A, Krzeszowiak; Baran, Jarosław; Hyszko, Mariola; Ruggiero, Irena; Wieckiewicz, J; Stachura, Jerzy; Zembala, Marek

doi:10.1002/jlb.65.5.597

Cited by 9 publications

(4 citation statements)

References 41 publications

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“…As previously described [20], cells were stained with anti-CD 14 mAbs and were fixed and permeabilized. Then these cells were stained with FITC-conjugated anti-iNOS antibody (BD Biosciences, Mountain View, CA) and were analyzed immediately using a FACSCalibur flow cytometer and CellQuest software (BD Biosciences, Mountain View, CA).…”

Section: Intracellular Inos Expression In Monocytesmentioning

confidence: 99%

Endotoxemia contributes to the immune paralysis in patients with cirrhosis

Lin

Tsai

et al. 2007

Journal of Hepatology

134

123

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Section: Intracellular Inos Expression In Monocytesmentioning

confidence: 99%

Endotoxemia contributes to the immune paralysis in patients with cirrhosis

Lin

Tsai

et al. 2007

Journal of Hepatology

134

123

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“…Moreover, tumor cells inhibit the production of reactive oxygen intermediates by macrophages [22]. A rather inconsistent pattern emerges from the studies on the influence of tumor cells on NO release by the monocyte-macrophage lineage; stimulatory in the case of leukaemia, lymphoma, mastocytoma [23][24][25], ascites hepatoma [26], fibrosarcoma [27], and colon carcinoma cells [28,29]; inhibitory in the case of mammary carcinoma [30,31] and murine melanoma [32].…”

Section: Introductionmentioning

confidence: 99%

Enhancement of Nitric Oxide Release in Mouse Inflammatory Macrophages Co-cultivated with Tumor Cells of a Different Origin

Calorini

Bianchini

Mannini

et al. 2005

Clin Exp Metastasis

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In the present study we investigated whether synthesis of nitric oxide (NO) by macrophages is affected by contact with tumor cells. Although it is well known that NO generated by macrophages influences different activities related to tumor progression, there is limited information on the modulatory role of tumor cells on NO release by macrophages. The experimental protocol used in our study consisted in the determination of NO secreted by macrophages, either resident or inflammatory, co-cultivated with tumor cells (B16 melanoma and L929 fibrosarcoma cells) at different cell densities and macrophage:tumor cell ratios. This experimental in vitro protocol simulates the different interactions between macrophages and tumor cells that occur during the development of a tumor mass. We found that the co-cultivation with tumor cells induced an increased secretion of NO in macrophages provided that they express an inflammatory phenotype, and they were challenged with LPS or IFNgamma/LPS. Two more variables were found to be critical in the increase of NO generation in inflammatory macrophages cultivated with tumor cells: a high cell density and a prevalence of tumor cells over macrophages. The enhancement of NO secreted in inflammatory macrophages stimulated by tumor cells was not observed in normal murine fibroblasts co-cultivated with tumor cells.

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“…It is conceivable that the different degrees of contact between macrophages and tumor cells during the different stages of tumor growth are relevant to the host cell/tumor cell relationship. Upon contact with tumor cells, macrophages release a range of mediators, including tumor necrosis factor a [14,15], nitric oxide [16,17], prostaglandin E 2 [15,18,19]. While nitric oxide and tumor necrosis factor a are cytotoxic for tumor cells [20,21], prostaglandin E 2 facilitates the escape of tumors from immune control by inhibiting T lymphocyte and macrophage activities [22].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of lipoxygenase pathway in macrophages co-cultivated with tumor cells

et al. 2005

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Although there is a great deal of interest in the role played by tumor-associated macrophages in tumor progression, the knowledge of the biological mediators involved in the interplay between macrophages and tumor cells is still limited. In the present study, we investigated whether the lipoxygenase pathway in resident murine peritoneal macrophages is affected by contact with tumor cells of a different origin, e.g. murine B16 melanoma and L929 fibrosarcoma cells, and human Hs294T melanoma and HT1080 fibrosarcoma cells. Our experiments have been carried out by using macrophages co-cultivated with tumor cells at different ratios, in order to simulate the relative proportions between macrophages and tumor cells during the in vivo development of a tumor. Reverse phase HPLC analyses of the lipoxygenase products of resident peritoneal macrophages revealed a rather complex profile characterized by a high level of 12(S)-hydroxyeicosatetraenoic acid and 15(S)-hydroxyeicosatetraenoic acid followed by leukotriene B(4), 5(S)-hydroxyeicosatetraenoic acid, and lipoxins. Macrophages co-cultivated with tumor cells, both murine and human, showed a marked reduction of lipoxygenase products, mainly in the co-cultures where tumor cells prevailed over macrophages. The characteristic profile of macrophage lipoxygenase products was re-established after removal of tumor cells from the co-cultures. The inhibitory effect on lipoxygenase pathways exerted by tumor cells, was not seen when macrophages were co-cultivated with normal primary murine and human fibroblasts.

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Demonstration of iNOS-mRNA and iNOS in human monocytes stimulated with cancer cells in vitro

Cited by 9 publications

References 41 publications

Endotoxemia contributes to the immune paralysis in patients with cirrhosis

Endotoxemia contributes to the immune paralysis in patients with cirrhosis

Enhancement of Nitric Oxide Release in Mouse Inflammatory Macrophages Co-cultivated with Tumor Cells of a Different Origin

Inhibition of lipoxygenase pathway in macrophages co-cultivated with tumor cells

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