• The Korean Journal of Malacology
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• v.32 no.4
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• pp.241-247
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• 2016

Macrophage Migration Inhibitory Factor (MIF) are well-defined role as unique cytokine and critical mediator in acute and chronic inflammatory diseases, autoimmune diseases. In this study, we isolated and characterized a full-length of MIF cDNA from the abalone (Haliotis discus hannai). The full-length cDNA of abMIF was of 1264 bp, consisting of a 5'-terminal UTR of 143 bp, an open reading frame of 360 bp and a 3-terminal UTR of 761 bp. The abalone MIF cDNA encodes a 119-amino acid polypeptide with a calculated molecular mass of 13.4 kDa and isoelectric point of 9.07. Multiple alignments and phylogenetic analysis with the deduced abalone MIF protein and showed strong homology with disk abalone (Haliotis discusdiscus). The deduced amino acid sequence of abMIF exhibited homology with other reported MIFs, such as 80%, with that of other disk abalone H. discus discus MIF gene. Quantitative real-time PCR (qRT-PCR) analysis indicated that abMIF was highly expression observed in hapatopacreas, intestine, foot, and gonad of normal conditioned abalone. Even though AbMIF mRNA level in hemocytes was low under the normal condition, it was sharply up-regulated and reached the maximum at 6 h post-infection with Vibrio parahaemolyticus, and then decreased at 24 h post-infection. This result indicates that abMIF plays an important role in responding in the innate immune system.

• Clinical and Experimental Reproductive Medicine
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• v.32 no.3
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• pp.287-293
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• 2005

Objective: To evaluate the usefulness of serum concentrations of macrophage migration inhibitory factor (MIF) of patients with ovarian cysts for differential diagnosis of endometrioama. Method: From Jan. 2003 to Dec. 2004, preoperative serum MIF levels were assessed in 28 women with endometrioma, 32 with benign epithelial tumor, 23 with functional and simple cysts, 22 with benign mature cystic teratoma, and 25 women without ovarian tumor as control. MIF levels were determined using an ELISA (Quantikine Human MIF immunoassay, R&D Systems, Inc., USA). Results: Mean MIF levels were higher in all groups with benign tumors than control (all p<0.01), but there was no significant difference between benign tumor groups (p=0.95). There was no significant correlation between MIF levels and tumor volume, body mass index (BMI) (p=0.635, 0.674 respectively) Serum MIF level had significant correlation with count of WBC and neutrophils (p=0.008, 0.024 respectively), but had no correlation with count of lymhocytes and monocytes (p=0.688, 0.294 respectively). Conclusions: This study showed a marked increase in MIF concentrations in the peripheral blood of patients with endometrioma, but there was no significant difference with other benign tumors. Serum MIF level had significant correlation with count of WBC and neutrophils. These suggest serum MIF level has no usefulness for differential diagnosis of endometrioma from other benign ovarian cysts.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.1737-1744
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• 2012

Macrophage migration inhibitory factor (MIF) is a pluripotent cytokine which plays roles in inflammation, immune responses and cancer development. It assists macrophages in carrying out functions like phagocytosis, adherence and motility. Of late, MIF is implicated in almost all stages of neoplasia and expression is a feature of most types of cancer. The presence of MIF in almost all tumors and all stages of cancer makes it an interesting candidate for cancer therapy. This review explores the roles of MIF in neoplasia.

• Journal of Life Science
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• v.15 no.6 s.73
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• pp.961-967
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• 2005

Macrophage migration inhibitory fartor (MIF), known as a cytokine, is a multifunctional protein that is ubiquitously expressed in a variety of cells and tissues; however, enzymatic function of MIF still remains elusive in cells. In this study, we assessed details of the tautomerase activity of MIF. We established rapid purification condition for MIF by using pGEX system and compared the L-dopachrome tautomerase activity of GST-MIF, tMIF, and MIF. The results show that GST (glutathione S-transferase)-epitope tag or N-terminal amino acids flanking the essential $P^{2}$ almost completely abrogated L-dopachrome tautomerase activity of MIF. Subsequently, to determine whether the N-terminal tags have effects on oligomerization of MIF, protein cross-linking products were analyzed on $15\%$ SDS-PACE. The result demonstrates that N-terminal tags are dispensable for the formation of MIF's homooligomers. Thus, the results imply that exposure of If containing hydrophobic pocket in the active site is critical for L-dopachrome tautomerase activity of MIF. In addition, our study suggest that the MIF's tautomerase activity might be influenced by interacting with cellular partners.

• Molecules and Cells
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• v.26 no.2
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• pp.193-199
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• 2008

The pro-apoptotic Bcl-2 family member Bim acts as a sensor for apoptotic stimuli and initiates apoptosis through the mitochondrial pathway. To identify novel regulators of Bim, we employed the yeast two-hybrid system and isolated the human gene encoding macrophage migration inhibitory factor (MIF), a ubiquitously expressed proinflammatory mediator that has also been implicated in cell proliferation, the cell cycle and carcinogenesis. The interaction between MIF and Bim was confirmed by both in vitro and in vivo protein interaction assays. Intriguingly, protein complexes between MIF and the three major Bim isoforms (BimEL/BimL/BimS) could be detected in HEK293 and K562 cells, especially in cells undergoing apoptosis. Moreover, exogenous expression of MIF partially inhibited Bim-induced apoptosis in HEK293 cells. SiRNA-mediated knockdown of MIF increased apoptosis in K562 cells exposed to the chemical oxidant diamide. Endogenous MIF may regulate the pro-apoptotic activity of Bim and inhibit the release of cytochrome c from mitochondria.

• Microbiology and Biotechnology Letters
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• v.48 no.4
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• pp.569-573
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• 2020

Brucellosis is a zoonotic disease caused by Brucella infections and humans usually contract this disease from close contact with infected animals or their products, usually via the ingestion of cheese or crude milk. Macrophage migration inhibitory factor (MIF) and Pro- and anti-inflammatory cytokines play an important role in susceptibility/resistance and the immunopathogenesis of Brucella infection. These cytokines are crucial factors in the initiation and progression of protective immunity against Brucella infection but the role of MIF has not been well studied in the human response to intracellular microbes. This study was designed to investigate the effect of MIF expression on Brucella susceptibility. A total of 85 positive rose Bengal tests and 24 samples from healthy individuals were collected for this study and subjected to polymerase chain reaction assays (PCR) of the bcsp31 diagnostic gene. MIF concentrations were evaluated using Enzyme-Linked immunosorbent assay (ELISA) and the results showed that 46 (54%) of the rose Bengal test samples were positive and 39 (46%) were negative for bcsp31 (p ≤ 0.05) and used as the gold standard for all of the comparisons in this study. The ELISA results indicate that the mean concentration of MIF was significantly higher in patients with positive rose Bengal tests when compared to the control groups and that its concentration increases with increasing age in both the patient and control groups (p ≤ 0.05).

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.23 no.1
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• pp.63-71
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• 2020

Purpose: Autoimmune hepatitis (AIH) is a chronic disease that may lead to cirrhosis. The immunopathogenesis of AIH is not fully understood and it mainly involves T-cell mediated mechanism. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine that promotes T cell response and its polymorphism may serve as a severity marker of AIH. No previous study has considered investigating MIF polymorphism in children with AIH. Methods: Forty-two children with definite diagnosis of AIH were enrolled along with 100 age and sex matched controls. All participants were tested for polymorphism at -173GC (rs755622) of MIF gene. All patients received the standard protocol of steroid plus azathioprine to achieve remission. Liver biopsy was performed at time of diagnosis for all patients and only 18 of them underwent a second biopsy after treatment. Results: No statistically significant differences in the frequency of the genotypes GG and GC or in allele distribution were found in both patient and control groups (p=0.590, 0.640 respectively). Initial alanine aminotransferase (ALT) levels at the time of presentation was significantly higher in the GC group than GG group (p=0.020). GC genotype significantly correlated with disease relapse (r=0.41, p=0.007). Regression of necroinflammation and the fibrosis score in the second liver biopsy was statistically significant in the GG group (p<0.0001, p=0.010 respectively). Conclusion: MIF -173GC polymorphism is associated with clinically significant markers of pediatric AIH, including increased initial serum ALT levels, may help predict necroinflammatory/fibrosis regression effectively, following immunosuppressive treatment.

• Journal of Trauma and Injury
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• v.31 no.3
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• pp.166-173
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• 2018

Purpose: Many traumatic patients die from sepsis and multiple organ failure. Early recognition of post-traumatic sepsis in traumatic patients will help improve the prognosis. Recently, procalcitonin (PCT), macrophage migration inhibitory factor (MIF), and lactic acid have emerged as predictive factors. Our study aims to explore the significance of PCT, MIF and lactic acid as a predictor of posttraumatic-sepsis in trauma patients. Methods: This study was conducted on prospective observational study patients who visited an emergency medical center in a university hospital from March 2014 to February 2016. We measured the white blood cells, c-reactive protein (CRP), lactic acid, PCT, and MIF with serum taken from the patient's blood within 1 hour of the occurrence of the trauma. The definition of post-traumatic sepsis was defined as being part of systemic inflammation response syndrome criteria with infections within a week. Results: A total of 132 patients were analyzed, wherein 74 patients were included in the low injury severity score (ISS) group (ISS <15) and 58 patients were included in the high ISS group (ISS ${\geq}15$). The mean PCT, MIF, and lactic acid levels were higher in the high ISS group (p<0.05). Meanwhile, 38 patients were included in the early sepsis group and 94 patients were included in the non-sepsis group. The mean MIF levels were higher in the sepsis group than the non-sepsis group (p<0.05) and there were no significant differences in the initial CRP, lactic acid, and PCT levels in these two groups. Conclusions: MIF may be considered as a predictive factor for sepsis in trauma patients.

• IMMUNE NETWORK
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• v.7 no.1
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• pp.39-47
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• 2007

Background: Stromal cell-derived factor (SDF)-1 is a potent chemoattractant for activated T cells into the inflamed Rheumatoid arthritis (RA) synovium. To determine the effect of macrophage migration inhibitory factor (MIF) on the production of SDF-1 in the inflamed RA synovium. Methods: The expression of SDF-1 and MIF in RA and Osteoarthritis (OA) synovium was examined by immunohistochemical staining. The SDF-1 was quantified by RT-PCR and ELISA after RA fibroblast like synoviocyte (FLS) were treated with MIF in the presence and absence of inhibitors of intracellular signal molecules. The synovial fluid (SF) and serum levels of MIF and SDF-1 in RA, OA and healthy control were measured by ELISA. Results: Expression of SDF-1 and MIF in synovium was higher in RA patients than in OA patients. The production of SDF-1 was enhanced in RA FLS by MIF stimulation. Such effect of MIF was blocked by the inhibitors of NF-${\kappa}B$. Concentrations of SDF-1 in the serum and SF were higher in RA patients than in OA patients and healthy control. SDF-1 and MIF was overexpressed in RA FLS, and MIF could up-regulate the production of SDF-1 in RA FLS via NF-${\kappa}B$-mediated pathways. Conclusion: These results suggest that an inhibition of interaction between MIF from T cells and SDF-1 of FLS may provide a new therapeutic approach in the treatment of RA.

• Journal of Physiology & Pathology in Korean Medicine
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• v.24 no.2
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• pp.242-248
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• 2010

The present study was designed in order to determine whether Lonicerae flos (LF) could mitigate rheumatoid arthritis through inhibition of cyclooxygenase (COX)-2 and matrix metalloproteinase (MMP)-9 by regulation of macrophage migration inhibitory factor (MIF). We found that MIF mRNA expression in synoviocytes stimulated with phorbol-12-myristate-13-acetate dose-dependantly decreased by LF extract treatment (0.4 - 1.0 mg/$m{\ell}$). The distribution of MIF, COX-2 and MMP-9 positive reacted cells in LPS induced arthritis of mice were decreased by LF (45 mg/kg/day) treatment for 28 days. These data likely indicate that LF may act as MIF inhibitor and may be possible to develop useful agent for rheumatoid arthritis.