Production of Monocyte Chemotactic Protein‐1 By Rat Brain Macrophages

Calvo, Charles‐Félix; Yoshimura, Teizo; Gelman, Michèle; Mallat, Michel

doi:10.1111/j.1460-9568.1996.tb01316.x

Cited by 93 publications

(56 citation statements)

References 53 publications

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“…IL-6 is a potent inducer of MCP-1 expression and is secreted by primary peripheral blood mononuclear cells (5) and brain macrophages (7). The low IL-6 levels following infection of Csf1 op /Csf1 op mice, together with the reduced numbers of Kupffer cells in these mice, could result in the lower MCP-1 synthesis observed in mutant mice.…”

Section: Discussionmentioning

confidence: 99%

Aberrant Macrophage and Neutrophil Population Dynamics and Impaired Th1 Response toListeria monocytogenesin Colony-Stimulating Factor 1-Deficient Mice

Guleria

Pollard

2001

Infect Immun

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Listeria monocytogenes, a facultative intracellular bacterium, has been used extensively to study innate immune responses. Macrophages act as hosts for this bacterium as well as a major defense against it. Using mice homozygous for a null mutation (Csf1 op ) in the gene for the mononuclear phagocytic growth factor colony-stimulating factor 1 (CSF-1), we have demonstrated that CSF-1-regulated macrophages were essential to defend against a listerial infection. In the absence of CSF-1, monocytes were not recruited to the sites of infection due to the lack of synthesis of the macrophage chemoattractant chemokine MCP-1. In addition, there was no burst of interleukin-10 (IL-10) synthesis that has been shown to result in the egress of neutrophils from sites of infection. Consequently, neutrophils were not replaced by macrophages, and numerous neutrophilfilled microabscesses developed, followed by tissue destruction and death of the mice. In the CSF-1 nullizygous mice compared to wild-type mice, there was also a very low synthesis of gamma interferon (IFN-␥), resulting in reduced macrophage activation. However, the concentrations of the IFN-␥-inducing cytokines IL-12 and IL-18 at this bacterial load were similar in these mutant mice. In contrast, IL-6 concentrations were dramatically reduced. Administration of IL-6 to Csf1 op /Csf1 op mice significantly increased the synthesis of IFN-␥ and reduced the bacterial burden to a greater extent than treatment with IFN-␥ alone. These data indicate that IL-6 occupies a central role in the CSF-1-regulated macrophage response to L. monocytogenes.

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Section: Discussionmentioning

confidence: 99%

Aberrant Macrophage and Neutrophil Population Dynamics and Impaired Th1 Response toListeria monocytogenesin Colony-Stimulating Factor 1-Deficient Mice

Guleria

Pollard

2001

Infect Immun

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“…37 Briefly, the cell suspension was cul- tured in DMEM supplemented with 2 mm l-glutamine, 20 mm NaHCO 3 , 5 U/ml penicillin, 50 g/ml streptomycin and 10% heat-inactivated fetal calf serum. All cell culture reagents were from Life Technologies (Cergy Pontoise, France).…”

Section: Primary Cultures Of Brain-derived Macrophages (Bm) and Bone mentioning

confidence: 99%

“…Bone marrow cells were collected from femurs and tibias of old male Long-Evans rats (Janvier, Le Genest-StIsle, France) as previously described. 37,38 Briefly, cells were flushed out with a 25-gauge needle into ice-cold phosphate-buffered saline (PBS) without Mg ++ , Ca…”

Section: Primary Cultures Of Brain-derived Macrophages (Bm) and Bone mentioning

confidence: 99%

Brain engraftment of autologous macrophages transduced with a lentiviral flap vector: an approach to complement brain dysfunctions

et al. 2002

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Transplantation of ex vivo gene-corrected autologous cells represents an attractive therapeutic approach for brain diseases. Among the cells of the central nervous system, brain macrophages are promising candidates due to their role in tissue homeostasis and their implication in several neurological diseases. Up to now, gene transfer into macrophages has proven difficult by most currently available gene delivery methods. We describe herein, an efficient transduction of rat bone marrow-derived and brain macrophages with an HIV-1-derived vector containing a central DNA flap and encoding the GFP reporter gene (TRIP-⌬U3-GFP). In primary cultures of macrophages our results show that more than 90% of the cells were transduced by the TRIP vector and that GFP

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“…37 The timing of leukocytosis after the injection of TNF-␣ into the brain is consistent with systemic increases of CCL-2 in the liver and the blood. CCL-2 has been shown to stimulate migration of bone marrow macrophages in vitro, 38 but hitherto there had been no in vivo demonstration that CCL-2 can induce a leukocytosis. In this study, we show that intravenous injection of CCL-2 causes a selective elevation in the number of circulating monocytes.…”

Section: Hepatically Released Chemokines Stimulate a Leukocytosismentioning

confidence: 99%

Central Nervous System Injury Triggers Hepatic CC and CXC Chemokine Expression that Is Associated with Leukocyte Mobilization and Recruitment to Both the Central Nervous System and the Liver

Campbell

Perry

Pitossi

et al. 2005

The American Journal of Pathology

142

156

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The administration of interleukin-1␤ to the brain induces hepatic CXC chemokine synthesis, which increases neutrophil levels in the blood, liver, and brain. We now show that such hepatic response is not restricted to the CXC chemokines. CCL-2, a CC chemokine, was released by the liver in response to a tumor necrosis factor (TNF)-␣ challenge to the brain and boosted monocyte levels. Furthermore, a clinically relevant compression injury to the spinal cord triggered hepatic chemokine expression of both types. After a spinal cord injury, elevated CCL-2 and CXCL-1 mRNA and protein were observed in the liver by TaqMan reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay as early as 2 to 4 hours. Simultaneously, we observed elevated levels of these chemokines and circulating leukocyte populations in the blood. Leukocytes were recruited to the liver at this early stage, whereas at the site of challenge in the central nervous system, few were observed until 24 hours. Artificial elevation of blood CCL-2 triggered dose-dependent monocyte mobilization in the blood and enhanced monocyte recruitment to the brain after TNF-␣ challenge. Attenuation of hepatic CCL-2 production with corticosteroids resulted in reduced monocyte levels after the TNF-␣ challenge. Thus, combined production of CC and CXC hepatic chemokines appears to amplify the After acute injury in the rodent brain, one of the earliest events is the hepatic release of regulatory acute-phase proteins, which occurs before there is any evidence of an inflammatory response in the brain.

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Production of Monocyte Chemotactic Protein‐1 By Rat Brain Macrophages

Cited by 93 publications

References 53 publications

Aberrant Macrophage and Neutrophil Population Dynamics and Impaired Th1 Response toListeria monocytogenesin Colony-Stimulating Factor 1-Deficient Mice

Aberrant Macrophage and Neutrophil Population Dynamics and Impaired Th1 Response toListeria monocytogenesin Colony-Stimulating Factor 1-Deficient Mice

Brain engraftment of autologous macrophages transduced with a lentiviral flap vector: an approach to complement brain dysfunctions

Central Nervous System Injury Triggers Hepatic CC and CXC Chemokine Expression that Is Associated with Leukocyte Mobilization and Recruitment to Both the Central Nervous System and the Liver

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