Differential Effects of Tyrosine Kinase Inhibitors on Tumor Necrosis Factor and Nitric Oxide Production by Murine Macrophages

Orlicek, Shari L.; Meals, Elizabeth; English, B. Keith

doi:10.1093/infdis/174.3.638

Cited by 28 publications

(30 citation statements)

References 14 publications

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“…Their activation is crucial to the progression of multiple inflammatory diseases such as septic shock, chronic inflammation, and atherosclerosis, via the release of inflammatory and cytotoxic mediators like cytokines or NO (Tamir and Tannenbaum 1996). In the present study, we have shown that exposing macrophages to LPS and IFN-c simultaneously induces a synergistic effect in terms of NO production as well as TNF-a secretion, in accordance with other authors (Orlicek et al 1996).…”

Section: Resultssupporting

confidence: 92%

Potential anti-inflammatory, anti-adhesive, anti/estrogenic, and angiotensin-converting enzyme inhibitory activities of anthocyanins and their gut metabolites

et al. 2012

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Epidemiological studies have indicated a positive association between the intake of foods rich in anthocyanins and the protection against cardiovascular diseases. Some authors have shown that anthocyanins are degraded by the gut microflora giving rise to the formation of other breakdown metabolites, which could also contribute to anthocyanin health effects. The objective of this study was to evaluate the effects of anthocyanins and their breakdown metabolites, protocatechuic, syringic, gallic, and vanillic acids, on different parameters involved in atherosclerosis, including inflammation, cell adhesion, chemotaxis, endothelial function, estrogenic/anti-estrogenic activity, and angiotensin-converting enzyme (ACE) inhibitory activity. From the assayed metabolites, only protocatechuic acid exhibited a slight inhibitory effect on NO production and TNF-a secretion in LPS-INF-c-induced macrophages. Gallic acid caused a decrease in the secretion of MCP-1, ICAM-1, and VCAM-1 in endothelial cells. All anthocyanins showed an ACE-inhibitory activity. Delphinidin-3-glucoside, pelargonidin-3-glucoside, and gallic acid showed affinity for ERb and pelargonidin and peonidin-3-glucosides for ERa. The current data suggest that anthocyanins and their breakdown metabolites may partly provide a protective effect against atherosclerosis that is multi-causal and involves different biochemical pathways. However, the concentrations of anthocyanins and their metabolites, as used in the present cell culture and in vitro assays mediating anti-inflammatory, anti-adhesive, antiestrogenic, and angiotensin-converting enzyme inhibitory activities, were often manifold higher than those physiologically achievable.

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Section: Resultssupporting

confidence: 92%

Potential anti-inflammatory, anti-adhesive, anti/estrogenic, and angiotensin-converting enzyme inhibitory activities of anthocyanins and their gut metabolites

et al. 2012

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“…We showed here that addition of PGE 2 to the cocultures of mycoplasma-infected YAC-1 cells and macrophages significantly decreased TNF production but has no effect on NO release nor on YAC-1 cell cytotoxicity. These results suggest that mycoplasma-induced TNF and NO production are differentially regulated and corroborate the view that different pathways are involved in generation of these two molecules as suggested by Zhang and Morrison [29] and Orlicek et al [30]. The mechanisms involved in NO and TNF induction by mycoplasmas are poorly understood.…”

Section: Discussionsupporting

confidence: 89%

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

Ribeiro‐Dias

Russo

Barbuto

et al. 1999

Journal of Leukocyte Biology

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Bacterial products stimulate macrophage tumoricidal activity through release of tumor necrosis factor (TNF) and nitric oxide (NO). We show here that thioglycollate-elicited macrophages acquire cytotoxic activity when cocultured with Mycoplasma arginini-infected YAC-1 tumor cells and release TNF and NO. Fixed mycoplasmainfected cells, supernatants from infected-cell cultures, or purified heat-killed mycoplasma obtained from cell-free cultures were all able to induce TNF and NO production. Thus, the mycoplasma per se and not a product of infected cells induce the release of these molecules. Addition of prostaglandin E 2 (PGE 2 ) to the cocultures, which reduced TNF release, or antibodies to TNF, did not affect macrophage cytotoxicity nor NO release. Inhibition of NO production by L-NAME or aminoguanidine reduced the cytotoxicity, and treatment with a NO donor was toxic to YAC-1 cells. These results indicate that M. arginini activates thioglycollateelicited murine macrophages for NO and TNF release increasing their cytotoxic activity toward YAC-1 cells and that this activity is dependent on NO but not TNF release. J. Leukoc. Biol. 65: 808-814; 1999.

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“…LPS alone is a weak stimulus for iNOS production by RAW 264.7 cells unless very high concentrations (e.g., Ն100 ng/mL) of LPS are used [12,15]. rIFN-␥ alone triggers iNOS accumulation by these cells in a dose-dependent fashion, but combinations of LPS and rIFN-␥ lead to synergistic accumulation of iNOS mRNA and protein [12,15].…”

Section: Murine Macrophagesmentioning

confidence: 99%

“…LPS alone is also a potent stimulus for TNF production, whereas rIFN-␥ alone stimulates relatively small amounts of TNF secretion by these cells [12,15].…”

Section: Murine Macrophagesmentioning

confidence: 99%

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Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity

Knapp

English

2000

Journal of Leukocyte Biology

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In macrophages, bacterial lipopolysaccharide (LPS) has been noted to mimic certain effects of the sphingolipid ceramide, suggesting that ceramide may be involved in macrophage activation by LPS and/or that LPS utilizes ceramiderelated signaling pathways. Putative downstream targets of ceramide include a ceramide-activated (serine/threonine) protein kinase (CAPK) and phosphatase (CAPP). However, the potential role of tyrosine phosphorylation pathways in macrophage response to ceramide has not been examined. Herein we report that cell-permeable analogs of ceramide up-regulate both inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) production in RAW 264.7 murine macrophages. Herbimycin A and genistein, potent natural inhibitors of protein tyrosine (but not serine/threonine) phosphorylation, block ceramide-induced iNOS and TNF production. Furthermore, the highly srcfamily selective pyrazolopyrimidine inhibitor PP1 also blocks ceramide-induced iNOS and TNF production in RAW 264.7 cells. We found that PP1 also inhibits ceramide-mediated tyrosine phosphorylation of the src-family kinase hck. These data indicate that src-related tyrosine kinases play a critical role in macrophage activation by ceramide.

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Differential Effects of Tyrosine Kinase Inhibitors on Tumor Necrosis Factor and Nitric Oxide Production by Murine Macrophages

Cited by 28 publications

References 14 publications

Potential anti-inflammatory, anti-adhesive, anti/estrogenic, and angiotensin-converting enzyme inhibitory activities of anthocyanins and their gut metabolites

Potential anti-inflammatory, anti-adhesive, anti/estrogenic, and angiotensin-converting enzyme inhibitory activities of anthocyanins and their gut metabolites

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

Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity

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