Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P80098 (monocyte chemoattractant protein)
 1,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consumption of isoflavone-containing foods such as soybean and soybean products has been reported to have beneficial effects on the cardiovascular system in postmenopausal women. The present study was carried out to examine the mechanism underlying the beneficial effects of isoflavones in apolipoprotein (apo) E-deficient mice subjected to ovarian resection. Compared with sham-operated mice, ovariectomized mice had a larger arterial lesion area in the aortic root. Feeding the ovariectomized mice an isoflavone-containing diet (0.055 mg/kJ of total isoflavones/cal of diet) reduced the size of these lesions more than did feeding them with an isoflavone-free diet. Neither ovariectomy nor diet had a significant effect on the concentration of cholesterol in serum and urinary levels of isoprostanes, which are biomarkers for oxidative stress in vivo. The ovariectomized mice showed a greater increase in mRNA abundance for monocyte chemoattractant protein (MCP)-I in the aorta and in the level of nitric oxide (NO) secreted by peritoneal macrophages in culture than did the sham-operated mice. The isoflavone-containing diet lowered the MCP-I expression and the NO secretion more than did the isoflavone-free diet. These results suggest that dietary isoflavones confer an antiatherogenic effect by preventing the activation of macrophages due to the removal of ovaries.
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PMID:Antiatherogenic effect of isoflavones in ovariectomized apolipoprotein e-deficient mice. 1790 22

Obese adipose tissue is characterized by an enhanced infiltration of macrophages. It is considered that the paracrine loop involving monocyte chemoattractant protein (MCP)-1 and tumor necrosis factor (TNF)-alpha between adipocytes and macrophages establishes a vicious cycle that augments the inflammatory changes and insulin resistance in obese adipose tissue. Polyphenols, which are widely distributed in fruit and vegetables, can act as antioxidants and some of them are also reported to have anti-inflammatory properties. Tomato is one of the most popular and extensively consumed vegetable crops worldwide, which also contains many flavonoids, mainly naringenin chalcone. We investigated the effect of flavonoids, including naringenin chalcone, on the production of proinflammatory mediators in lipopolysaccharide (LPS)-stimulated macrophages and in the interaction between adipocytes and macrophages. Naringenin chalcone inhibited the production of TNF-alpha, MCP-1, and nitric oxide (NO) by LPS-stimulated RAW 264 macrophages in a dose-dependent manner. Coculture of 3T3-L1 adipocytes and RAW 264 macrophages markedly enhanced the production of TNF-alpha, MCP-1, and NO compared with the control cultures; however, treatment with naringenin chalcone dose-dependently inhibited the production of these proinflammatory mediators. These results indicate that naringenin chalcone exhibits anti-inflammatory properties by inhibiting the production of proinflammatory cytokines in the interaction between adipocytes and macrophages. Naringenin chalcone may be useful for ameliorating the inflammatory changes in obese adipose tissue.
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PMID:Inhibitory effect of naringenin chalcone on inflammatory changes in the interaction between adipocytes and macrophages. 1791 59

Mycobacterium tuberculosis exerts its pathogenic effects mainly via its cell wall glycolipid called Mannosylated Lipoarabinomannan (Man-LAM), which subverts the cellular inflammatory responses by the suppression of superoxide anion generation in earlier hours, and nitric oxide (NO) generation at later hours of pathogenic invasion. In this paper, we have shown the prophylactic effect of C-C chemokines, both in vitro and in vivo. Exogenous administration of C-C chemokines, particularly monocyte chemoattractant protein (MCP)-1, led to the induction of superoxide anion generation via the restoration of impaired protein kinase C (PKC) signalling in Man-LAM-treated macrophages. Monocyte chemoattractant protein-1 could also potently induce NO generation by upregulation of the proinflammatory cytokines tumour necrosis factor-alpha and interleukin-12 from Man-LAM-treated macrophages accompanied by inhibition of anti-inflammatory responses. Our in vivo observations clearly exhibited effective restoration of impaired PKC signalling as well as proinflammatory cytokine expression by MCP-1 in Man-LAM treated as well as M. tuberculosis H37Rv-infected C57BL/6 mice. We also observed, as direct evidence, that MCP-1 induced a significant reduction of the number of viable tubercle bacilli in the lungs and spleen of infected mice. Collectively, our findings strongly suggest the effectiveness of MCP-1 as a potent immunoprophylactic tool for controlling the mycobacterial establishment within the host.
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PMID:Restoration of impaired free radical generation and proinflammatory cytokines by MCP-1 in mycobacterial pathogenesis. 1828 29

In response to bacterial challenges, fibroblasts, a major constituent of gingival connective tissue, can produce immunoregulatory cytokines and proteolytic enzymes that may contribute to tissue destruction and the progression of periodontitis, a chronic inflammatory disease affecting tooth-supporting tissues, including alveolar bone. The spirochete Treponema denticola is a major etiological agent of periodontitis and can invade oral tissues. The aim of the present study was to investigate the inflammatory response of gingival fibroblasts to T. denticola lipooligosaccharide (LOS). T. denticola LOS induced significant production of various inflammatory mediators by fibroblasts, including interleukin-6, interleukin-8, monocyte chemoattractant protein 1, nitric oxide, and prostaglandin E(2). In addition, the secretion of matrix metalloproteinase 3, an enzyme active on basement membrane components, was also significantly increased. The response of fibroblasts was dose-dependent and much stronger following a 24 h stimulation period. The expression and/or phosphorylation state of several signaling proteins, including Fos, MKK1, MKK2, MKK3/6, NF-kappaB p50, and NF-kappaB p65, was enhanced following stimulation of fibroblasts with T. denticola LOS. In summary, T. denticola LOS induced an inflammatory response in gingival fibroblasts and may thus contribute to the immunopathogenesis of periodontitis and the progression of the disease.
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PMID:Treponema denticola lipooligosaccharide activates gingival fibroblasts and upregulates inflammatory mediator production. 1836 71

Estrogen, a natural immunomodulatory compound, has been shown to promote the induction of a prototype T helper 1 cytokine, interferon (IFN)-gamma, as well as to up-regulate IFNgamma-mediated proinflammatory molecules (nitric oxide, cyclooxygenase 2, monocyte chemoattractant protein 1). Because IL-12 is a major IFNgamma-inducing cytokine, in this study we investigated whether estrogen treatment of wild-type C57BL/6 mice alters IL-12-mediated signaling pathways. A recent study has shown that IL-12 activates two isoforms of signal transducer and activation of transcription (STAT) 4, a normal-sized (full-length STAT4alpha) and a truncated form (STAT4beta). Interestingly, we found that estrogen treatment preferentially up-regulates the phosphorylation of STAT4beta in splenic lymphoid cells. Time kinetic data showed the differential activation of STAT4beta in splenic lymphoid cells from estrogen-treated mice, but not in cells from placebo controls. The activation of STAT4beta was mediated by IL-12 and not IFNgamma because deliberate addition or neutralization of IL-12, but not IFNgamma, affected the activation of STAT4beta. In contrast to IL-12-induced activation of STAT4beta in cells from estrogen-treated mice, STAT4alpha was not increased, rather it tended to be decreased. In this context, STAT4alpha-induced p27(kip1) protein was decreased in concanavalin A + IL-12-activated lymphocytes from estrogen-treated mice only. By using the in vitro DNA binding assay, we confirmed the ability of pSTAT4beta to bind to the IFNgamma-activated sites (IFNgamma activation sequences)/STAT4-binding sites in estrogen-treated mice. Our data are the first to show that estrogen apparently has selective effects on IL-12-mediated signaling by preferentially activating STAT4beta. These novel findings are likely to provide new knowledge with regard to estrogen regulation of inflammation.
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PMID:Signal transducer and activation of transcription (STAT) 4beta, a shorter isoform of interleukin-12-induced STAT4, is preferentially activated by estrogen. 1898 75

Anesthesia and surgical trauma are considered major oxidative and nitrosative stress effectors resulting in the development of SIRS. In this study we evaluated the usefulness of early enteral nutrition after surgical trauma. Sixty male Wistar rats were subjected to midline laparotomy and feeding-gastrostomy. Twenty of these rats served as controls after recovering from the operation stress. The remaining rats received, through gastrostomy, enteral nutrition or placebo-feeding for 24 h. Oxidative stress markers and CC chemokine production were evaluated in rat serum and liver tissue. The operation itself was found to increase nitric oxide (NO) and malondialdehyde (MDA) and to decrease superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), as well as liver tissue energy charge (EC) in relation to controls. The rats receiving enteral feeding exhibited statistically significantly lower levels of NO and MDA, and higher levels of SOD, GSH-Px, and liver EC, in relation to placebo feeding rats. The operation significantly increased the chemokines monocyte chemoattractant protein (MCP)-1 and regulated upon activation, normal T-cell expressed, and secreted (RANTES) in rat serum, while enteral nutrition caused a further significant increase in chemokine levels in serum. mRNA chemokine expression in liver was increased in a similar pattern. These findings indicate that early enteral feeding might play an important role after surgery ameliorating oxidative stress, affecting positively the hepatic EC and regulating, via chemokine production, cell trafficking, and healing process.
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PMID:Oxidative stress due to anesthesia and surgical trauma: importance of early enteral nutrition. 1919 68

Sofalcone, 2'-carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy)chalcone, has been used as an anti-ulcer agent, although its precise molecular mechanism has not been completely understood. In the current study, we tested the effects of sofalcone on the inflammatory crosstalk between macrophages and adipocytes and on the differentiation of pre-adipocytes. We found that sofalcone has a strong suppressive effect on the production of nitric oxide (NO), tumor necrosis factor (TNF)alpha, and monocyte chemoattractant protein (MCP)-1 in the culture medium of a coculture system containing RAW264.7 macrophages and 3T3-F442A adipocytes stimulated with lipopolysaccharide (LPS). The suppressive effect of sofalcone on NO production was attenuated by treatment with tin-protoporphyrin (SnPP), a heme-oxygenase (HO)-1 inhibitor. Western blotting analysis showed that sofalcone increased HO-1 expression in both 3T3-F442A mature adipocytes and undifferentiated fibroblasts. Sofalcone also inhibited the differentiation of 3T3-F442A pre-adipocytes into adipocytes, which was restored by SnPP treatment. These results suggest that sofalcone has preferable properties for obesity or metabolic syndrome.
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PMID:Sofalcone, an anti-ulcer chalcone derivative, suppresses inflammatory crosstalk between macrophages and adipocytes and adipocyte differentiation: implication of heme-oxygenase-1 induction. 1923 4

Healing of the burn wound is a critical component of the burn patient's successful recovery. While inflammation is a critical component of the healing process, it is unknown whether the inflammatory response differs between non-burn and burn wounds. To study this, mice were subjected to major burn injury or sham procedure. Wound cells were collected by implantation of polyvinyl alcohol sponges beneath the burn site in injured mice or beneath uninjured skin in sham mice (i.e., non-burn wound). Three days thereafter, skin, wound fluid, and infiltrating cells were collected for analysis. Significant levels of tumor necrosis factor (TNF)-alpha, interleukin (IL-6), monocyte chemoattractant protein (MCP)-1, and keratinocyte-derived chemokine (KC) were observed in burn wound tissue and the wound fluid from both non-burn and burn wounds. Burn injury induced 3-fold higher levels of KC and 50-fold higher levels of IL-6 in the wound fluid compared with non-burn injury. Significant numbers of the cells from both burn and non-burn wounds were CD11b(+), GR1(+), and F4/80(+), suggestive of a myeloid suppressor cell phenotype, whereas CD3(+) T-cells were negligible under both conditions. LPS induced TNF-alpha, IL-6, IL-10, MCP-1, KC, and nitric oxide production in both cell populations, however, IL-6, IL-10, MCP-1, and KC levels were suppressed in burn wound cell cultures. These findings indicate that significant differences in the wound inflammatory response exist between burn and non-burn cutaneous wounds and that the unique characteristics of the inflammatory response at the burn site may be an important contributing factor to post-burn wound healing complications.
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PMID:Impact of thermal injury on wound infiltration and the dermal inflammatory response. 1939 37

4-Methylnitrosamino-1-(3-pyridyl)-1-butanone (NNK) is a tobacco-specific procarcinogen. We have investigated whether NNK causes inflammatory upheaval in the brain by activation of resident microglia and astrocyte and result in bystander neuronal damage. We have carried out the work in both in vitro and in vivo models. We have found that treatment with NNK causes significant activation of mouse microglial (BV2) cell line as evident by increase in reactive oxygen species and nitric oxide level. Western blot analysis has showed increase in proinflammatory signaling proteins, proinflammatory effector proteins, and other stress-related proteins. Interestingly, increased levels of proinflammatory cytokines like interleukin (IL)-6, tumor necrosis factor-alpha, monocyte chemoattractant protein 1 (MCP1), and IL-12p70 are also detected. Work from our in vivo studies has demonstrated similar increase in proinflammatory signaling and effector molecules along with the proinflammatory cytokine levels, following NNK treatment. Immunohistochemical staining of the brain sections of NNK-treated mice reveals massive microglial and astrocyte activation along with distinct foci of neuronal damage. Both in vitro and in vivo results provide strong indication that NNK causes significant upheaval of the inflammatory condition of brain and inflicts subsequent neuronal damage.
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PMID:Tobacco carcinogen induces microglial activation and subsequent neuronal damage. 1950 Feb 13

The critical impairments of innate and adaptive immunity that cause susceptibility to mucosal candidiasis in human immunodeficiency virus (HIV) infection have not been fully determined. We therefore conducted an analysis of macrophage-mediated responses to Candida albicans in transgenic (Tg) mice expressing Nef, Env, and Rev of HIV type 1 (HIV-1) in CD4(+) T cells, dendritic cells, and macrophages and developing an AIDS-like disease (CD4C/HIV(MutA) Tg mice). Macrophages were successfully recruited to the oral and gastric mucosae of these Tg mice in response to chronic carriage of C. albicans and displayed polarization toward an alternatively activated phenotype. Functionally, peritoneal macrophages from uninfected Tg mice exhibited increased phagocytosis of C. albicans and enhanced production of interleukin 6 and monocyte chemoattractant protein 1, demonstrating that the HIV-1 transgene independently activates selected macrophage functions. Production of H(2)O(2) by macrophages from Tg mice primed with gamma interferon and treated with phorbol 12-myristate 13-acetate or C. albicans was moderately reduced, but expression of the HIV-1 transgene did not alter production of nitric oxide or reduce killing of C. albicans. A knockout of the inducible nitric oxide synthase (NOS2) gene in these Tg mice did not augment oral or gastrointestinal burdens during chronic carriage of C. albicans or cause systemic dissemination, likely due to a redundancy provided by partially preserved production of H(2)O(2) and oxygen-independent candidacidal mechanisms. Thus, the macrophage response to C. albicans is largely preserved in these Tg mice, and no functional macrophage defect appears to primarily determine the susceptibility to mucosal candidiasis.
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PMID:Macrophage-mediated responses to Candida albicans in mice expressing the human immunodeficiency virus type 1 transgene. 1956 79


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