Increased serum levels of macrophage migration inhibitory factor in alcoholic liver diseases and their expression in liver tissues

Kumagi, Teru; Akbar, Fazle; Horiike, Norio; Onji, Morikazu

doi:10.1016/s0009-9120(01)00214-4

Cited by 39 publications

(35 citation statements)

References 19 publications

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“…It was reported that MIF staining was observed in hepatocytes of liver specimens from patients with liver cirrhosis . Kumagi et al (2001) described an increase of MIF levels in serum and localization of MIF-expressing cells in the liver in patients with alcoholic hepatitis. On the other hand, it was reported that macrophages might act as an early trigger in the genesis of hepatic fibrosis (Noda et al 1996;Yamate et al 1999).…”

Section: Discussionmentioning

confidence: 99%

“…In liver disease, necrosis and inflammation in ethanol-fed rats are associated with increased expression of MIF (Nanji et al 2001). Moreover, Kumagi et al (2001) reported that MIF was expressed by hepatocytes and by the infiltrating cells in specimens from patients with alcoholic hep-atitis. These reports suggested that MIF was an important mediator of the inflammatory response in liver disease.…”

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confidence: 99%

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Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Hori

Sato²,

Yamate³

et al. 2009

Eur J Histochem

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Macrophage migration inhibitory factor (MIF) is a molecule known to regulate macrophage accumulation at sites of inflammation. To elucidate the role of MIF in progression of liver fibrosis, the immunohistochemical localization of MIF and macrophages in the liver were examined. Male Wistar rats received thioacetamide (TA) injections (200 mg/kg, i.p.) for 1 or 6 weeks. In biochemical and histological tests, it was confirmed that liver fibrosis was induced. In immunohistochemical analyses, the expression of MIF protein was seen in hepatocytes in the areas extending out from the central veins to the portal tracts. In particular, at 6 weeks, immunoreactivity was detected in degenerated hepatocytes adjacent to the fibrotic areas but hardly observed in the fibrotic areas. On the other hand, a number of exudate macrophages stained by antibody ED1 were seen in the areas from the central veins to the portal tracts at 1 week and in the fibrotic areas at 6 weeks. Macrophages also showed a significant increase in number as compared with controls. These results revealed that there was a close relationship between the appearance of MIF expression and ED1-positive exudate macrophages in degenerated hepatocytes during the progression of TA-induced liver fibrosis

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Hori

Sato²,

Yamate³

et al. 2009

Eur J Histochem

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“…MIF is released from the pancreatic islets in a glucose-dependent fashion (Waeber et al 1997, Johansson et al 2003, Allaman-Pillet et al 2004, and potentiates the glucose-induced release of insulin from b-cells in an autocrine loop (Waeber et al 1997). In addition, MIF is produced by many peripheral tissues, where it induces an alteration of glucose metabolism especially during the inflammatory response (Benigni et al 2000, Kumagi et al 2001, Atsumi et al 2007. While most of these studies were performed in the setting of stress, several reports have also documented an association between MIF, obesity, and insulin resistance (IR) in a physiological environment.…”

Section: Introductionmentioning

confidence: 99%

Macrophage migration inhibitory factor deficiency leads to age-dependent impairment of glucose homeostasis in mice

Serre‐Beinier

Toso²,

Morel³

et al. 2010

Journal of Endocrinology

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Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine produced by many cells and tissues including pancreatic b-cells, liver, skeletal muscle, and adipocytes. This study investigates the potential role of MIF in carbohydrate homeostasis in a physiological setting outside of severe inflammation, utilizing Mif knockout (MIFK/K) mice. Compared with wild-type (WT) mice, MIFK/K mice had a lower body weight, from birth until 4 months of age, but subsequently gained weight faster, resulting in a higher body weight at 12 months of age. The lower weight in young mice was related to a higher energy expenditure, and the higher weight in older mice was related to an increased food intake and a higher fat mass. Fasting blood insulin level was higher in MIFK/K mice compared with WT mice at any age. After i.p. glucose injection, the elevation of blood insulin level was higher in MIFK/K mice compared with WT mice, at 2 months of age, but was lower in 12-month-old MIFK/K mice. As a result, the glucose clearance during intraperitoneal glucose tolerance tests was higher in MIFK/K mice compared with WT mice until 4 months of age, and was lower in 12-month-old MIFK/K mice. Insulin resistance was estimated (euglycemic-hyperinsulinemic clamp tests), and the phosphorylation activity of AKT was similar in MIFK/K mice and WT mice. In conclusion, this mouse model provides evidence for the role of MIF in the control of glucose homeostasis.

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“…Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator, which plays a pivotal role in inflammatory and immune diseases (1)(2)(3)(4)(5). It contributes toward an excessive inflammatory response both directly via an induction of proinflammatory cytokine secretion (6) and indirectly through its ability to override the anti-inflammatory activity of glucocorticoids (7).…”

Section: Introductionmentioning

confidence: 99%

Functional polymorphisms in the promoter region of macrophage migration inhibitory factor and chronic gastritis

Arisawa

Tahara²,

Shibata³

et al. 2007

Int J Mol Med

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Abstract. Macrophage migration inhibitory factor (MIF) is a key proinflammatory mediator, which plays a pivotal role in inflammatory and immune diseases. We attempted to clarify associations of the functional polymorphisms of the MIF gene promoter with the development of chronic gastritis. The study was performed with 290 stocked DNAs from subjects with no evidence of gastric malignancy. We employed the PCR-SSCP method to detect gene polymorphisms. The severity of histological chronic gastritis in antral biopsy specimens was classified according to the updated Sydney system. Both the 7/7-CATT repeat at position -794 and the -173 C/C genotypes were significantly associated with a risk of developing severe gastric mucosal atrophy (OR, 9.69; 95% CI, 1.29-72.5; and OR, 4.60; 95% CI, 1.05-20.2, respectively). In subjects younger than 60 years old, the number of 7-CATT alleles was significantly correlated with both the activity and inflammation scores (p=0.0079 and 0.0080, respectively). Our results suggested that functional promoter polymorphisms of the MIF gene might be associated with the severity of gastric mucosal inflammation in younger subjects and with the subsequent development of mucosal atrophy.

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Increased serum levels of macrophage migration inhibitory factor in alcoholic liver diseases and their expression in liver tissues

Cited by 39 publications

References 19 publications

Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Immunohistochemical study of macrophage migration inhibitory factor in rat liver fibrosis induced by thioacetamide

Macrophage migration inhibitory factor deficiency leads to age-dependent impairment of glucose homeostasis in mice

Functional polymorphisms in the promoter region of macrophage migration inhibitory factor and chronic gastritis

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