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            },
            "creatorSummary": "Reckelhoff et al.",
            "parsedDate": "1999-05",
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        },
        "data": {
            "key": "X8ERZMIH",
            "version": 86,
            "itemType": "journalArticle",
            "title": "Chronic aminoguanidine attenuates renal dysfunction and injury in aging rats",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Jane F",
                    "lastName": "Reckelhoff"
                },
                {
                    "creatorType": "author",
                    "firstName": "Bettye Sue",
                    "lastName": "Hennington"
                },
                {
                    "creatorType": "author",
                    "firstName": "Vijaya",
                    "lastName": "Kanji"
                },
                {
                    "creatorType": "author",
                    "firstName": "Lorraine C",
                    "lastName": "Racusen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ann Marie",
                    "lastName": "Schmidt"
                },
                {
                    "creatorType": "author",
                    "firstName": "Shi Du",
                    "lastName": "Yan"
                },
                {
                    "creatorType": "author",
                    "firstName": "Jason",
                    "lastName": "Morrow"
                },
                {
                    "creatorType": "author",
                    "firstName": "L.Jackson",
                    "lastName": "Roberts II"
                },
                {
                    "creatorType": "author",
                    "firstName": "Abdulla K",
                    "lastName": "Salahudeen"
                }
            ],
            "abstractNote": "We have previously shown that aging is associated with increased lipid peroxidation, reductions in renal function, and increased glomerular sclerosis. The mechanism(s) responsible for these age-related changes are not clear. The purpose of the present studies was to determine if there was an increase in inducible nitric oxide synthase (iNOS) with aging, and if so, whether inhibition of iNOS would prevent aging injury by preventing free radical-mediated lipid peroxidation. iNOS protein expression in the kidney increased by approximately 90% by 24 months. Inhibition of iNOS by aminoguanidine (0.1% in drinking water) for 9 months, beginning at 13 months of age, reduced blood pressure, improved glomerular filtration rate by 70%, and renal plasma flow by 40%, whereas glomerular sclerosis was considerably reduced. Renal F2-isoprostanes and malondialdehyde levels, markers of oxidative stress and lipid peroxidation, were not reduced by aminoguanidine. Aminoguanidine also did not attenuate immunostaining for advanced glycosylation end products (AGE) in the kidneys. These findings suggest that aminoguanidine attenuates aging renal dysfunction by inhibiting a pathophysiologic function of iNOS that is independent of free radical-mediated lipid peroxidation or significant effects on AGE deposition.",
            "publicationTitle": "American Journal of Hypertension",
            "publisher": "",
            "place": "",
            "date": "May 1999",
            "volume": "12",
            "issue": "5",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "492-498",
            "series": "",
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            "journalAbbreviation": "American Journal of Hypertension",
            "DOI": "10.1016/S0895-7061(98)00264-7",
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            "url": "http://www.sciencedirect.com/science/article/pii/S0895706198002647",
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            "tags": [
                {
                    "tag": "F2-isoprostanes"
                },
                {
                    "tag": "advanced glycosylation end products"
                },
                {
                    "tag": "free radicals"
                },
                {
                    "tag": "glomerular filtration rate"
                },
                {
                    "tag": "lipid peroxidation"
                },
                {
                    "tag": "renal plasma flow"
                }
            ],
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            "dateAdded": "2016-03-20T23:10:19Z",
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    {
        "key": "SNSZUZHE",
        "version": 85,
        "library": {
            "type": "group",
            "id": 470057,
            "name": "Macrophage Phenotyping",
            "links": {
                "alternate": {
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            },
            "creatorSummary": "Chang et al.",
            "parsedDate": "2001-02-02",
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            "version": 85,
            "itemType": "journalArticle",
            "title": "Macrophage Arginase Promotes Tumor Cell Growth and Suppresses Nitric Oxide-mediated Tumor Cytotoxicity",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Chiung-I",
                    "lastName": "Chang"
                },
                {
                    "creatorType": "author",
                    "firstName": "James C.",
                    "lastName": "Liao"
                },
                {
                    "creatorType": "author",
                    "firstName": "Lih",
                    "lastName": "Kuo"
                }
            ],
            "abstractNote": "Macrophages use l-arginine to synthesize nitric oxide (NO)\nand polyamines through the inducible NO synthase (iNOS) and arginase,\nrespectively. The released NO contributes to the tumoricidal activity\nof macrophages, whereas polyamines may promote the growth of tumor\ncells. Both the tumoricidal and growth-promoting activities from\nmacrophages have been reported; however, the underlying mechanisms for\nswitching between this dual function of macrophages remain unclear.\nHere, we test the hypothesis that arginase participates in the\nswitching between the cytotoxic and growth-promoting activities of\nmacrophages toward tumor cells. To alter arginase activity in\nmacrophages, cells (murine macrophage cell line J774A.1) were\ntransfected with the rat liver arginase gene or treated with an\narginase inhibitor, l-norvaline. The effects of macrophage\narginase activity on the growth-promoting and cytotoxic activities of\nmacrophages toward breast tumor cells (ZR-75–1) were investigated in a\ncoculture system. The results demonstrated that overexpression of\narginase in macrophages enhanced l-ornithine and putrescine\nproduction and consequently promoted tumor cell proliferation. This\nproliferative effect was down-regulated by the arginase inhibitor\nl-norvaline. Furthermore, increases in arginase activity\nalso attenuated NO production by the lipopolysaccharide-activated\nmacrophages and thus reduced the cytotoxic effect on cocultured tumor\ncells. Inhibiting arginase activity by l-norvaline\neffectively reversed the suppression of NO-mediated tumor cytotoxicity.\nTogether, these results suggest that arginase induction in macrophages\ncan enhance tumor cell growth by providing them with polyamines and\nsuppress tumor cytotoxicity by reducing NO production. It appears that\nl-arginine metabolism through the arginase and iNOS\npathways in macrophages can have very different influences on the\ngrowth of nearby tumor cells depending on which pathway is prevailing.",
            "publicationTitle": "Cancer Research",
            "publisher": "",
            "place": "",
            "date": "February 2, 2001",
            "volume": "61",
            "issue": "3",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "1100-1106",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Cancer Research",
            "DOI": "",
            "citationKey": "",
            "url": "http://cancerres.aacrjournals.org/content/61/3/1100.abstract",
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            "relations": {},
            "dateAdded": "2016-03-20T17:52:28Z",
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    {
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        "version": 78,
        "library": {
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            "id": 470057,
            "name": "Macrophage Phenotyping",
            "links": {
                "alternate": {
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                }
            },
            "creatorSummary": "Meltzer et al.",
            "parsedDate": "1997-04-01",
            "numChildren": 0
        },
        "data": {
            "key": "DS8V5G6S",
            "version": 78,
            "itemType": "journalArticle",
            "title": "Enhanced Immunohistochemical Detection of Autonomic Nerve Fibers, Cytokines and Inducible Nitric Oxide Synthase by Light and Fluorescent Microscopy in Rat Spleen",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Jon C.",
                    "lastName": "Meltzer"
                },
                {
                    "creatorType": "author",
                    "firstName": "Paul C.",
                    "lastName": "Grimm"
                },
                {
                    "creatorType": "author",
                    "firstName": "Arnold H.",
                    "lastName": "Greenberg"
                },
                {
                    "creatorType": "author",
                    "firstName": "Dwight M.",
                    "lastName": "Nance"
                }
            ],
            "abstractNote": "We have developed enhanced immunohistochemical protocols for detecting autonomic nerve fibers and splenocyte-associated proteins in rat spleen. This includes norepinephrine-synthesizing enzymes (dopamine-βeta hydroxylase (DBH) and tyrosine hydroxylase (TH)), neuropeptide Y (NPY), tumor necrosis factor -α (TNF-α), interferon-γ (IFN-γ), c-fos protein, inducible nitric oxide synthase (iNOS), and the macrophage cell marker ED1. Animals were divided into sham-operated and splenic nerve-sectioned groups for detection of DBH, TH, and NPY. For immunodetection of TNF-α, iNOS, IFN-γ and c-fos, animals were injected IV with saline or 100 μg of lipopolysaccharide (LPS) and were sacrificed at various time intervals post injection. Rats were perfused with 4% paraformaldehyde, spleens removed and cryoprotected, and 50-μm floating sections were cut on a freezing microtome. Immunodetection was performed with various detection systems and substrate/chromogen solutions, and in some cases using pretreatment with proteinase K (PK) for antigen unmasking. PK pretreatment increased immunostaining for DBH, TH, NPY, IFN-γ, iNOS, and ED1, and the improvement was concentration-dependent. Using NPY immunostaining to index the signal-to-noise ratio for various substrates and detection systems, we found that an alkaline phosphatase detection system with NBT/BCIP as a substrate was the best procedure for light microscopy, whereas the CY3-labeled secondary antibody technique proved optimal for fluorescent microscopy. Surgical transection of the splenic nerve eliminated all nerve fiber staining for DBH, TH, and NPY. TNF-α, IFN-γ, c-fos, and iNOS proteins were observed in the spleen in a time-dependent manner after LPS stimulation. Fluorescent double labeling, visualized with fluorescent confocal scanning laser microscopy, revealed many NPY fibers distributed among the ED1-labeled macrophages. These results demonstrate that immunohistochemistry can be used to index the activational effects of an immune challenge on splenocytes in situ and verifies that splenic immune cells are innervated by the sympathetic nervous system.",
            "publicationTitle": "Journal of Histochemistry & Cytochemistry",
            "publisher": "",
            "place": "",
            "date": "April 1, 1997",
            "volume": "45",
            "issue": "4",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "599-610",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Journal of Histochemistry & Cytochemistry",
            "DOI": "10.1177/002215549704500412",
            "citationKey": "",
            "url": "http://jhc.sagepub.com/content/45/4/599.abstract",
            "accessDate": "",
            "PMID": "",
            "PMCID": "",
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            ],
            "relations": {},
            "dateAdded": "2016-03-20T16:18:34Z",
            "dateModified": "2016-03-20T16:18:34Z"
        }
    },
    {
        "key": "TU2MP8VC",
        "version": 77,
        "library": {
            "type": "group",
            "id": 470057,
            "name": "Macrophage Phenotyping",
            "links": {
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                }
            },
            "creatorSummary": "Chiang et al.",
            "parsedDate": "2008-02-01",
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        },
        "data": {
            "key": "TU2MP8VC",
            "version": 77,
            "itemType": "journalArticle",
            "title": "Functional phenotype of macrophages depends on assay procedures",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Chi-Shiun",
                    "lastName": "Chiang"
                },
                {
                    "creatorType": "author",
                    "firstName": "Fang-Hsin",
                    "lastName": "Chen"
                },
                {
                    "creatorType": "author",
                    "firstName": "Ji-Hong",
                    "lastName": "Hong"
                },
                {
                    "creatorType": "author",
                    "firstName": "Pei-Shin",
                    "lastName": "Jiang"
                },
                {
                    "creatorType": "author",
                    "firstName": "Hsiang-Ling",
                    "lastName": "Huang"
                },
                {
                    "creatorType": "author",
                    "firstName": "Chun-Chieh",
                    "lastName": "Wang"
                },
                {
                    "creatorType": "author",
                    "firstName": "William H.",
                    "lastName": "McBride"
                }
            ],
            "abstractNote": "Macrophages display different phenotypes that can switch in response to their micro-environment. In our earlier study (Chiang, C. S., Liu, W. C. and Jung, S. M., 2005. Compartmental responses after thoracic irradiation of mice: strain differences. Int. J. Radiat. Oncol. Biol. Phys. 62:862) on radiation-induced cytokine expression in lung lavage samples, there was a suggestion that the procedures used to harvest lung macrophages affected the profiles they expressed. To further explore this issue, we examined gene expression by cell populations, mainly macrophages, isolated by lavage from lung and peritoneal cavity following either in vivo or in vitro stimulation with LPS, IFN-γ or irradiation. We found that expression of mRNA for tumor necrosis factor-alpha, IL-1α/β and IL-6 varied several fold depending on whether the assay was performed on cells immediately after isolation or after in vitro manipulation. The relative level of inducible nitric oxide synthase (iNOS) to arginase I (Arg I), which is frequently used as index of the M1 versus M2 functional macrophage phenotype, also varied. LPS stimulation in vivo was able to change the profile from Arg I expression to one where the iNOS pathway became dominant, but was unable to do this in vitro. This contrasts with the ability of IFN-γ to generate an iNOS-dominant pathway in vitro, but not in vivo. This study cautions that the expression of inflammatory cytokines and the iNOS to Arg I ratio, which is often used as an index of their functional capacity, varies with the experimental conditions.",
            "publicationTitle": "International Immunology",
            "publisher": "",
            "place": "",
            "date": "February 1, 2008",
            "volume": "20",
            "issue": "2",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "215-222",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "International Immunology",
            "DOI": "10.1093/intimm/dxm137",
            "citationKey": "",
            "url": "http://intimm.oxfordjournals.org/content/20/2/215.abstract",
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            "relations": {},
            "dateAdded": "2016-03-09T22:30:46Z",
            "dateModified": "2016-03-09T22:30:46Z"
        }
    },
    {
        "key": "GHZKD45S",
        "version": 75,
        "library": {
            "type": "group",
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            "links": {
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                    }
                }
            },
            "creatorSummary": "Sassy-Prigent et al.",
            "parsedDate": "2000-03-01",
            "numChildren": 0
        },
        "data": {
            "key": "GHZKD45S",
            "version": 75,
            "itemType": "journalArticle",
            "title": "Early glomerular macrophage recruitment in streptozotocin-induced diabetic rats.",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "C",
                    "lastName": "Sassy-Prigent"
                },
                {
                    "creatorType": "author",
                    "firstName": "D",
                    "lastName": "Heudes"
                },
                {
                    "creatorType": "author",
                    "firstName": "C",
                    "lastName": "Mandet"
                },
                {
                    "creatorType": "author",
                    "firstName": "M F",
                    "lastName": "Bélair"
                },
                {
                    "creatorType": "author",
                    "firstName": "O",
                    "lastName": "Michel"
                },
                {
                    "creatorType": "author",
                    "firstName": "B",
                    "lastName": "Perdereau"
                },
                {
                    "creatorType": "author",
                    "firstName": "J",
                    "lastName": "Bariéty"
                },
                {
                    "creatorType": "author",
                    "firstName": "P",
                    "lastName": "Bruneval"
                }
            ],
            "abstractNote": "Diabetic glomerulosclerosis is defined by increased glomerular extracellular matrix (ECM) that is mainly synthesized by mesangial cells that underwent an activation mediated by cytokines and growth factors from various cellular origins. In this study, we tested whether macrophages could infiltrate the glomeruli and influence ECM synthesis in experimental diabetes. To test our hypothesis, we initially studied the dynamics of glomerular macrophage recruitment in streptozotocin-induced diabetic rats at days 1, 2, 4, 8, 15, and 30 by using quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) on isolated glomeruli and immunohistochemistry and morphometry. We then assessed the role of macrophages on the basis of the pharmacological modulation of their recruitment by insulin or ACE inhibitor treatments and by X-irradiation-induced macrophage depletion at days 8 and 30. Macrophages were recruited within the glomeruli at the very early phase of hyperglycemia by using RT-PCR CD14 detection from day 2 and by using ED1 immunohistochemistry from day 8. This glomerular macrophage infiltration was associated with an increase in alpha1-chain type IV collagen mRNA. In parallel, the diabetic glomeruli became hypertrophic with an increase in the mesangial area. Macrophage recruitment was preceded by or associated with an increased glomerular expression of vascular cell adhesion molecule 1, intracellular adhesion molecule 1, and monocyte chemoattractant protein 1, which contributes to monocyte diapedesis. Glomerular interleukin-1beta mRNA synthesis was also enhanced as early as day 1 and could be involved in the increase in ECM and adhesion molecule gene expressions. Insulin treatment and irradiation-induced macrophage depletion completely prevented the glomerular macrophage recruitment and decreased alpha1-chain type IV collagen mRNA and mesangial area in diabetic rats, whereas ACE inhibitor treatment had an incomplete effect. It can be concluded that in the streptozotocin model, hyperglycemia is followed by an early macrophage recruitment that contributes to the molecular and structural events that could lead to glomerulosclerosis. Therefore, besides direct stimulation of mesangial cells by hyperglycemia, macrophages recruited in the glomeruli during the early phase of hyperglycemia could secondarily act on mesangial cells.",
            "publicationTitle": "Diabetes",
            "publisher": "",
            "place": "",
            "date": "March 1, 2000",
            "volume": "49",
            "issue": "3",
            "section": "",
            "partNumber": "",
            "partTitle": "",
            "pages": "466-475",
            "series": "",
            "seriesTitle": "",
            "seriesText": "",
            "journalAbbreviation": "Diabetes",
            "DOI": "10.2337/diabetes.49.3.466",
            "citationKey": "",
            "url": "http://diabetes.diabetesjournals.org/content/49/3/466.abstract",
            "accessDate": "",
            "PMID": "",
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            "ISSN": "",
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            "title": "Caspase-3 Mediates the Pathogenic Effect of Yersinia pestis YopM in Liver of C57BL/6 Mice and Contributes to YopM's Function in Spleen",
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                    "firstName": "Mikael",
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            "abstractNote": "The virulence protein YopM of the plague bacterium Yersinia pestis has different dominant effects in liver and spleen. Previous studies focused on spleen, where YopM inhibits accumulation of inflammatory dendritic cells. In the present study we focused on liver, where PMN function may be directly undermined by YopM without changes in inflammatory cell numbers in the initial days of infection, and foci of inflammation are easily identified. Mice were infected with parent and ΔyopM-1 Y. pestis KIM5, and effects of YopM were assessed by immunohistochemistry and determinations of bacterial viable numbers in organs. The bacteria were found associated with myeloid cells in foci of inflammation and in liver sinusoids. A new in-vivo phenotype of YopM was revealed: death of inflammatory cells, evidenced by TUNEL staining beginning at d 1 of infection. Based on distributions of Ly6G(+), F4/80(+), and iNOS(+) cells within foci, the cells that were killed could have included both PMNs and macrophages. By 2 d post-infection, YopM had no effect on distribution of these cells, but by 3 d cellular decomposition had outstripped acute inflammation in foci due to parent Y. pestis, while foci due to the ΔyopM-1 strain still contained many inflammatory cells. The destruction depended on the presence of both PMNs in the mice and YopM in the bacteria. In mice that lacked the apoptosis mediator caspase-3 the infection dynamics were novel: the parent Y. pestis was limited in growth comparably to the ΔyopM-1 strain in liver, and in spleen a partial growth limitation for parent Y. pestis was seen. This result identified caspase-3 as a co-factor or effector in YopM's action and supports the hypothesis that in liver YopM's main pathogenic effect is mediated by caspase-3 to cause apoptosis of PMNs.",
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            "abstractNote": "Studies on monocyte and macrophage biology and differentiation have revealed the pleiotropic activities of these cells. Macrophages are tissue sentinels that maintain tissue integrity by eliminating/repairing damaged cells and matrices. In this M2-like mode, they can also promote tumor growth. Conversely, M1-like macrophages are key effector cells for the elimination of pathogens, virally infected, and cancer cells. Macrophage differentiation from monocytes occurs in the tissue in concomitance with the acquisition of a functional phenotype that depends on microenvironmental signals, thereby accounting for the many and apparently opposed macrophage functions. Many questions arise. When monocytes differentiate into macrophages in a tissue (concomitantly adopting a specific functional program, M1 or M2), do they all die during the inflammatory reaction, or do some of them survive? Do those that survive become quiescent tissue macrophages, able to react as naïve cells to a new challenge? Or, do monocyte-derived tissue macrophages conserve a “memory” of their past inflammatory activation? This review will address some of these important questions under the general framework of the role of monocytes and macrophages in the initiation, development, resolution, and chronicization of inflammation.",
            "publicationTitle": "Frontiers in Immunology",
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            "pages": "514",
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    {
        "key": "HC672QPJ",
        "version": 55,
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            "title": "Spleen-derived macrophages are readily polarized into classically activated (M1) or alternatively activated (M2) states",
            "creators": [
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                    "creatorType": "author",
                    "firstName": "Rylend",
                    "lastName": "Mulder"
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                {
                    "creatorType": "author",
                    "firstName": "Andra",
                    "lastName": "Banete"
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                    "creatorType": "author",
                    "firstName": "Sameh",
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            ],
            "abstractNote": "Abstract\nBone marrow derived macrophages (BM-MΦ) that differentiate from precursor cells can be polarized into classically activated pro-inflammatory (M1) or alternatively activated (M2) states depending upon the cytokine microenvironment. We questioned whether tissue MΦ, such as spleen-derived MΦ (Sp-MΦ), have the ability to differentiate into M1 or M2 cells. We show in response to activation with IFN-gamma (IFN-γ) and lipopolysaccharide (LPS), that the Sp-MΦ readily acquired an M1 status indicated by up-regulation of iNOS mRNA, nitric oxide (NO) production, and the co-stimulatory molecule CD86. Conversely, Sp-MΦ exposed to IL-4 exhibited increased levels of mannose receptor (CD 206), arginase-1 (Arg)-1 mRNA expression, and significant urea production typical of M2 cells. At this stage of differentiation, the M2 Sp-MΦ were more efficient at phagocytosis of cell-associated antigens than their M1 counterparts. This polarization was not indefinite as the cells could revert back to their original state upon the removal of stimuli and exhibited flexibility to convert from M2 to M1. Remarkably, both M1 and M2 Sp-MΦ induced more CD4 expression on their cells surface after stimulation. We also demonstrate that adherent macrophages cultured for a short term in IL-4 enhances ARG-1 and YM-1 mRNA along with increasing urea producing capacity: traits indicative of an M2 phenotype. Moreover, in response to in vivo virus infection, the adherent macrophages obtained from spleens rapidly express iNOS. These results provide new evidence for the polarization capabilities of Sp-MΦ when exposed to pro-inflammatory or anti-inflammatory cytokines.",
            "publicationTitle": "Immunobiology",
            "publisher": "",
            "place": "",
            "date": "October 2014",
            "volume": "219",
            "issue": "10",
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            "partTitle": "",
            "pages": "737-745",
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            "journalAbbreviation": "Immunobiology",
            "DOI": "10.1016/j.imbio.2014.05.005",
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            "url": "http://www.sciencedirect.com/science/article/pii/S0171298514000977",
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            "tags": [
                {
                    "tag": "CD4"
                },
                {
                    "tag": "LCMV"
                },
                {
                    "tag": "MACROPHAGES"
                },
                {
                    "tag": "Phagocytosis"
                },
                {
                    "tag": "Spleen"
                }
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        "key": "9E9UQ66W",
        "version": 53,
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            "creatorSummary": "Li et al.",
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            "version": 53,
            "itemType": "journalArticle",
            "title": "Differences in iNOS and Arginase Expression and Activity in the Macrophages of Rats Are Responsible for the Resistance against T. gondii Infection",
            "creators": [
                {
                    "creatorType": "author",
                    "firstName": "Zhi",
                    "lastName": "Li"
                },
                {
                    "creatorType": "author",
                    "firstName": "Zhi-Jun",
                    "lastName": "Zhao"
                },
                {
                    "creatorType": "author",
                    "firstName": "Xing-Quan",
                    "lastName": "Zhu"
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                {
                    "creatorType": "author",
                    "firstName": "Qing-Shi",
                    "lastName": "Ren"
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                {
                    "creatorType": "author",
                    "firstName": "Fang-Fang",
                    "lastName": "Nie"
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                {
                    "creatorType": "author",
                    "firstName": "Jiang-Mei",
                    "lastName": "Gao"
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                {
                    "creatorType": "author",
                    "firstName": "Xiao-Jie",
                    "lastName": "Gao"
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                {
                    "creatorType": "author",
                    "firstName": "Ting-Bao",
                    "lastName": "Yang"
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                    "creatorType": "author",
                    "firstName": "Wen-Liang",
                    "lastName": "Zhou"
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                    "creatorType": "author",
                    "firstName": "Ji-Long",
                    "lastName": "Shen"
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                {
                    "creatorType": "author",
                    "firstName": "Yong",
                    "lastName": "Wang"
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                    "creatorType": "author",
                    "firstName": "Fang-Li",
                    "lastName": "Lu"
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                    "firstName": "Xiao-Guang",
                    "lastName": "Chen"
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                {
                    "creatorType": "author",
                    "firstName": "Geoff",
                    "lastName": "Hide"
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                {
                    "creatorType": "author",
                    "firstName": "Francisco J",
                    "lastName": "Ayala"
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                {
                    "creatorType": "author",
                    "firstName": "Zhao-Rong",
                    "lastName": "Lun"
                },
                {
                    "creatorType": "editor",
                    "firstName": "Anne Charlotte",
                    "lastName": "Gruner"
                }
            ],
            "abstractNote": "Toxoplasma gondii infects humans and warm blooded animals causing devastating disease worldwide. It has long been a mystery as to why the peritoneal macrophages of rats are naturally resistant to T. gondii infection while those of mice are not. Here, we report that high expression levels and activity of inducible nitric oxide synthase (iNOS) and low levels of arginase-1 (Arg 1) activity in the peritoneal macrophages of rats are responsible for their resistance against T. gondii infection, due to high nitric oxide and low polyamines within these cells. The opposite situation was observed in the peritoneal macrophages of mice. This discovery of the opposing functions of iNOS and Arg 1 in rodent peritoneal macrophages may lead to a better understanding of the resistance mechanisms of mammals, particularly humans and livestock, against T. gondii and other intracellular pathogens.",
            "publicationTitle": "PLoS ONE",
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            "itemType": "journalArticle",
            "title": "Macrophages in Kidney Injury, Inflammation, and Fibrosis",
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                    "firstName": "Qi",
                    "lastName": "Cao"
                },
                {
                    "creatorType": "author",
                    "firstName": "David C. H.",
                    "lastName": "Harris"
                },
                {
                    "creatorType": "author",
                    "firstName": "Yiping",
                    "lastName": "Wang"
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            ],
            "abstractNote": "Macrophages are found in normal kidney and in increased numbers in diseased kidney, where they act as key players in renal injury, inflammation, and fibrosis. Macrophages are highly heterogeneous cells and exhibit distinct phenotypic and functional characteristics in response to various stimuli in the local microenvironment in different types of kidney disease. In kidney tissue necrosis and/or infection, damage- and/or pathogen-associated molecular patterns induce pro-inflammatory macrophages, which contribute to further tissue injury, inflammation, and subsequent fibrosis. Apoptotic cells and anti-inflammatory factors in post-inflammatory tissues induced anti-inflammatory macrophages, which can mediate kidney repair and regeneration. This review summarizes the role of macrophages with different phenotypes in kidney injury, inflammation, and fibrosis in various acute and chronic kidney diseases. Understanding alterations of kidney microenvironment and the factors that control the phenotype and functions of macrophages may offer an avenue for the development of new cellular and cytokine/growth factor-based therapies as alternative treatment options for patients with kidney disease.",
            "publicationTitle": "Physiology",
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            "pages": "183-194",
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