Regulation of Nitric Oxide Production by Murine Peritoneal Macrophages Treated in Vitro with Chemokine Monocyte Chemoattractant Protein 1

Biswas, Subhra K.; Sodhi, Ajit; Paul, Saki

doi:10.1006/niox.2001.0370

Cited by 46 publications

(31 citation statements)

References 65 publications

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“…However, the aP2 promoter used in these experiments to drive transgenic Ccl2 expression is not specific for adipocytes and is also active in macrophages [29]. Since MCP-1 is known to activate macrophages [13,14], it is entirely feasible that the increased recruitment of macrophages into adipose tissue in these studies is facilitated by secretion of MCP-1 and other chemokines/cytokines by constitutively activated macrophages. One of these studies also found that a single intramuscular treatment with a plasmid encoding a human mutant form of Ccl2 (7ND), which dimerises with wild-type MCP-1 and inhibits its activity, was sufficient to reduce insulin resistance in obese db/db mice [27].…”

Section: Discussionmentioning

confidence: 99%

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Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

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Aims/hypothesis Tissue macrophage accumulation is thought to induce insulin resistance during obesity and stimulate the progression of diabetic nephropathy. Monocyte chemoattractant protein-1 (MCP-1) is a potent stimulator of macrophage recruitment. It is increased in adipose tissue during obesity and in diabetic kidneys, suggesting that inflammation of these tissues may be MCP-1-dependent. Based on these findings, the aim of this study was to examine whether a deficiency in MCP-1 would alter the development of type 2 diabetes and its renal complications. Materials and methods The role of MCP-1 in the progression of type 2 diabetes and its associated renal injury was assessed in obese db/db mice that were deficient in the gene encoding MCP-1 (Ccl2). Results The incidence and development of type 2 diabetes were similar in Ccl2 +/+ and Ccl2 −/− db/db mice between 8 and 32 weeks of age. Body mass, hyperglycaemia, hyperinsulinaemia, glucose and insulin tolerance, plasma triacylglycerol and serum NEFA were not different between these strains. Pathological changes in epididymal adipose tissue, including increases in macrophage accumulation and Tnfa mRNA and reductions in Adipoq mRNA, were unaffected by the absence of MCP-1. In contrast, kidney macrophage accumulation and the progression of diabetic renal injury (albuminuria, histopathology, renal fibrosis) were substantially reduced in Ccl2 −/− compared with Ccl2 +/+ db/db mice with equivalent diabetes. Conclusions/interpretation Our study demonstrates that MCP-1 promotes type 2 diabetic renal injury but does not influence the development of obesity, insulin resistance or type 2 diabetes in db/db mice. MCP-1 plays a critical role in inflammation of the kidney, but not adipose tissue, during the progression of type 2 diabetes.

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Section: Discussionmentioning

confidence: 99%

“…Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that is known to affect the accumulation and function of macrophages [12][13][14]. MCP-1 levels are increased in plasma and adipose tissue in mouse models of obesity [15,16], and correlate with the number of CD11b + monocytes in these animals [16].…”

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confidence: 99%

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

et al. 2006

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“…One of the candidates for such soluble factors would be MCP-1, because MCP-1 is produced not only by monocytes/macrophages but also by neutrophils (24), and because MCP-1 activates monocytes/macrophages to show an anti-tumor effect or to produce superoxide (25)(26)(27)(28)(29). Although MCP-1 protein production by thymic macrophages was significantly elevated 12 h after whole-body x-irradiation (data not shown), it is not known whether or not MCP-1 is also produced by neutrophils to enhance macrophage-mediated digestion of apoptotic cells.…”

Section: Discussionmentioning

confidence: 99%

Neutrophils Accelerate Macrophage-Mediated Digestion of Apoptotic Cells In Vivo as Well as In Vitro

Iyoda

Nagata

Akashi³

et al. 2005

The Journal of Immunology

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It is generally believed that the clearance of apoptotic cells does not lead to inflammation. In contrast, we previously found that injection of apoptotic cells into the peritoneal cavity induced the expression of an inflammatory chemokine, MIP-2, and infiltration of neutrophils, and that anti-MIP-2 Abs suppressed the infiltration significantly. Because our previous study showed that whole-body x-irradiation caused neutrophil infiltration into the thymus along with T cell apoptosis, we examined the role of neutrophils in apoptotic cell clearance. Neutrophil infiltration reached a peak 12 h after irradiation with 1 Gy of x-rays. Immunohistological analysis revealed that apoptotic cells disappeared dramatically from 10.5 to 12 h after x-irradiation. As neutrophils moved from an inner area of the cortex to the periphery, apoptotic cells disappeared concomitantly. Either anti-MIP-2 or anti-CXCR2 Abs suppressed neutrophil infiltration significantly, and the suppression of neutrophil infiltration by anti-MIP-2 Abs delayed the disappearance of apoptotic cells. Moreover, macrophage-mediated digestion of apoptotic thymocytes was accelerated in vitro on coculturing with neutrophils, even if neutrophils were separated from macrophages. These results suggest that neutrophils are recruited to the thymus mainly by MIP-2 after whole-body x-irradiation and that such neutrophils may not induce inflammation but rather accelerate complete digestion of apoptotic cells by macrophages.

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“…The significant production of IL-12 and TNF-α highlights the importance of these two cytokines during the early stages of infection, with IL-12 inducing the differentiation of Th1 lymphocytes and TNF-α activating iNOS. However, a low production of nitrite by these cells was observed, a finding that can be explained by the fact that the cultures basically consisted of monocytes, which are poor producers of nitrite in short-term culture 28 . Furthermore, studies using experimental models have shown that nitrite levels induced by TNF-α alone are not sufficient for an efficient trypanocidal action 18 .…”

Section: Conflict Of Interest Financial Support Referencesmentioning

confidence: 96%

Production of cytokine and chemokines by human mononuclear cells and whole blood cells after infection with Trypanosoma cruzi

Rezende-Oliveira

Sarmento

Rodrigues

2012

Rev. Soc. Bras. Med. Trop.

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INTRODUCTION: The innate immune response is the first mechanism of protection against Trypanosoma cruzi, and the interaction of inflammatory cells with parasite molecules may activate this response and modulate the adaptive immune system. This study aimed to analyze the levels of cytokines and chemokines synthesized by the whole blood cells (WBC) and peripheral blood mononuclear cells (PBMC) of individuals seronegative for Chagas disease after interaction with live T. cruzi trypomastigotes. METHODS: IL-12, IL-10, TNF-α, TGF-β, CCL-5, CCL-2, CCL-3, and CXCL-9 were measured by ELISA. Nitrite was determined by the Griess method. RESULTS: IL-10 was produced at high levels by WBC compared with PBMC, even after incubation with live trypomastigotes. Production of TNF-α by both PBMC and WBC was significantly higher after stimulation with trypomastigotes. Only PBMC produced significantly higher levels of IL-12 after parasite stimulation. Stimulation of cultures with trypomastigotes induced an increase of CXCL-9 levels produced by WBC. Nitrite levels produced by PBMC increased after the addition of parasites to the culture. CONCLUSIONS: Surface molecules of T. cruzi may induce the production of cytokines and chemokines by cells of the innate immune system through the activation of specific receptors not evaluated in this experiment. The ability to induce IL-12 and TNF-α contributes to shift the adaptive response towards a Th1 profile.

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Regulation of Nitric Oxide Production by Murine Peritoneal Macrophages Treated in Vitro with Chemokine Monocyte Chemoattractant Protein 1

Cited by 46 publications

References 65 publications

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Monocyte chemoattractant protein-1-induced tissue inflammation is critical for the development of renal injury but not type 2 diabetes in obese db/db mice

Neutrophils Accelerate Macrophage-Mediated Digestion of Apoptotic Cells In Vivo as Well as In Vitro

Production of cytokine and chemokines by human mononuclear cells and whole blood cells after infection with Trypanosoma cruzi

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