scholarly journals Modulatory Role of Macrophage Migration Inhibitory Factor on Cytokines and Clinical Features of Sarcoidosis

2022 ◽  
Author(s):  
Morvarid Elahi ◽  
Jaya Talreja ◽  
Laura L. Koth ◽  
Lobelia Samavati
Keyword(s):  
Clinical Features ◽  
Negative Correlation ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Macrophage Migration ◽  
Positive Correlation ◽  
Ifn Γ ◽  
Low Serum

Abstract Background: Sarcoidosis is a systemic granulomatous disease of unknown etiology with a significant heterogeneity in organ manifestations, severity, and clinical course. Subjects with sarcoidosis share several features such as, non-necrotizing granuloma, hypergammaglobulinemia, increased local and circulating inflammatory cytokines, such as interleukin (IL)-6, IL-18, and interferon gamma (IFN-γ). Macrophage migration inhibitory factor (MIF) is a pluripotent chemokine produced by various cell types. The expression of MIF at sites of inflammation suggests a regulatory role in the function of macrophages. The objective of this study was to investigate the role of MIF in the serum and bronchoalveolar lavage (BAL) fluid of sarcoidosis patients in association with clinical features and other cytokines. Methods: Sera and BALs of sarcoidosis patients (n=55) were collected at the time of diagnosis and patients were followed longitudinally for 3 years. Additionally, fifteen healthy controls participated in the study. The medical records of all patients including, demographics, radiography stages, pulmonary function tests, and organ involvements were recorded. The levels of MIF, IL-18, IL-10, IL-6, IFN-γ and lysozyme in serum and BAL samples were measured by ELISA. Statistical analyses were performed using SPSS software. Results: Serum MIF had a remarkable positive correlation with IL-10 and IFN-γ but had a negative correlation with serum IgG levels. Importantly, longitudinal follow-up showed a positive correlation between MIF and % predicted diffusion capacity (%DLCO) at 3-year. Serum IL-18 had a significant positive correlation with serum lysozyme, but a negative correlation with % predicted total lung capacity at 3-year follow up. We identified two groups of sarcoidosis subjects with distinct clinical and cytokine features. A group with prominent extrapulmonary involvement, and low serum MIF, IL-10 and IFN-γ levels and a group with elevated serum MIF, IL-10 and IFN-γ levels. Moreover, we found a negative correlation between BAL IL-18 and BAL MIF in sarcoidosis subjects.Conclusions: Patients with low serum MIF, IL-10 and IFN-γ levels has severe and mostly extrapulmonary sarcoidosis with elevated lysozyme and IL-18 levels. Our work provides understanding of phenotypic diversity in association with heterogeneity in cytokine landscape in sarcoidosis.

scholarly journals Modulatory Role of Macrophage Migration Inhibitory Factor on Cytokines and Clinical Features of Sarcoidosis

2021 ◽  
Author(s):  
Morvarid Elahi ◽  
Jaya Talreja ◽  
Laura L. Koth ◽  
Lobelia Samavati
Keyword(s):  
Clinical Features ◽  
Negative Correlation ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Macrophage Migration ◽  
Positive Correlation ◽  
Ifn Γ ◽  
Low Serum

Abstract Background: Sarcoidosis is a systemic granulomatous disease of unknown etiology with a significant heterogeneity in organ manifestations, severity, and clinical course. Subjects with sarcoidosis share several features such as, non-necrotizing granuloma, hypergammaglobulinemia, increased local and circulating inflammatory cytokines, such as interleukin (IL)-6, IL-18, and interferon gamma (IFN-γ). Macrophage migration inhibitory factor (MIF) is a pluripotent chemokine produced by various cell types. The expression of MIF at sites of inflammation suggests a regulatory role in the function of macrophages. The objective of this study was to investigate the role of MIF in the serum and bronchoalveolar lavage (BAL) fluid of sarcoidosis patients in association with clinical features and other cytokines. Methods: Sera and BALs of sarcoidosis patients (n=55) were collected at the time of diagnosis and patients were followed longitudinally for 3 years. Additionally, fifteen healthy controls participated in the study. The medical records of all patients including, demographics, radiography stages, pulmonary function tests, and organ involvements were recorded. The levels of MIF, IL-18, IL-10, IL-6, IFN-γ and lysozyme in serum and BAL samples were measured by ELISA. Statistical analyses were performed using SPSS software. Results: Serum MIF had a remarkable positive correlation with IL-10 and IFN-γ but had a negative correlation with serum IgG levels. Importantly, longitudinal follow-up showed a positive correlation between MIF and % predicted diffusion capacity (%DLCO) at 3-year. Serum IL-18 had a significant positive correlation with serum lysozyme, but a negative correlation with % predicted total lung capacity at 3-year follow up. We identified two groups of sarcoidosis subjects with distinct clinical and cytokine features. A group with prominent extrapulmonary involvement, and low serum MIF, IL-10 and IFN-γ levels and a group with elevated serum MIF, IL-10 and IFN-γ levels. Moreover, we found a negative correlation between BAL IL-18 and BAL MIF in sarcoidosis subjects.Conclusions: Patients with low serum MIF, IL-10 and IFN-γ levels has severe and mostly extrapulmonary sarcoidosis with elevated lysozyme and IL-18 levels. Our work provides understanding of phenotypic diversity in association with heterogeneity in cytokine landscape in sarcoidosis.

scholarly journals Role of Macrophage Migration Inhibitory Factor in the Regulatory T Cell Response of Tumor-Bearing Mice

2012 ◽  
Vol 189 (8) ◽  
pp. 3905-3913 ◽  
Author(s):  
Susanna Choi ◽  
Hang-Rae Kim ◽  
Lin Leng ◽  
Insoo Kang ◽  
William L. Jorgensen ◽  
...  
Keyword(s):  
T Cell ◽  
Migration Inhibitory Factor ◽  
Regulatory T Cell ◽  
Cell Response ◽  
Macrophage Migration Inhibitory Factor ◽  
T Cell Response ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Tumor Bearing

scholarly journals Macrophage migration inhibitory factor may play a protective role in osteoarthritis

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Ming Liu ◽  
Zikun Xie ◽  
Guang Sun ◽  
Liujun Chen ◽  
Dake Qi ◽  
...  
Keyword(s):  
Polymerase Chain Reaction ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Protective Role ◽  
Macrophage Migration ◽  
Chain Reaction ◽  
Protein Levels ◽  
Tnf Α ◽  
Polymerase Chain

Abstract Background Osteoarthritis (OA) is the most prevalent form of arthritis and the major cause of disability and overall diminution of quality of life in the elderly population. Currently there is no cure for OA, partly due to the large gaps in our understanding of its underlying molecular and cellular mechanisms. Macrophage migration inhibitory factor (MIF) is a procytokine that mediates pleiotropic inflammatory effects in inflammatory diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS). However, data on the role of MIF in OA is limited with conflicting results. We undertook this study to investigate the role of MIF in OA by examining MIF genotype, mRNA expression, and protein levels in the Newfoundland Osteoarthritis Study. Methods One hundred nineteen end-stage knee/hip OA patients, 16 RA patients, and 113 healthy controls were included in the study. Two polymorphisms in the MIF gene, rs755622, and -794 CATT5-8, were genotyped using polymerase chain reaction–restriction fragment length polymorphism (PCR-RFLP) and PCR followed by automated capillary electrophoresis, respectively. MIF mRNA levels in articular cartilage and subchondral bone were measured by quantitative polymerase chain reaction. Plasma concentrations of MIF, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β) were measured by enzyme-linked immunosorbent assay. Results rs755622 and -794 CATT5-8 genotypes were not associated with MIF mRNA or protein levels or OA (all p ≥ 0.19). MIF mRNA level in cartilage was lower in OA patients than in controls (p = 0.028) and RA patients (p = 0.004), while the levels in bone were comparable between OA patients and controls (p = 0.165). MIF protein level in plasma was lower in OA patients than in controls (p = 3.01 × 10−10), while the levels of TNF-α, IL-6 and IL-1β in plasma were all significantly higher in OA patients than in controls (all p ≤ 0.0007). Multivariable logistic regression showed lower MIF and higher IL-1β protein levels in plasma were independently associated with OA (OR per SD increase = 0.10 and 8.08; 95% CI = 0.04–0.19 and 4.42–16.82, respectively), but TNF-α and IL-6 became non-significant. Conclusions Reduced MIF mRNA and protein expression in OA patients suggested MIF might have a protective role in OA and could serve as a biomarker to differentiate OA from other joint disorders.

scholarly journals The role of human macrophage migration inhibitory factor in promoting angiogenesis

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
XiYong Yu ◽  
ZhiXin Shan ◽  
QiuXiong Lin ◽  
ShiXia Cai ◽  
Min Yang ◽  
...  
Keyword(s):  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Human Macrophage ◽  
Macrophage Migration

Role of macrophage migration inhibitory factor in bleomycin-induced lung injury and fibrosis in mice

2002 ◽  
Vol 283 (1) ◽  
pp. L156-L162 ◽  
Author(s):  
Yoshinori Tanino ◽  
Hironi Makita ◽  
Kenji Miyamoto ◽  
Tomoko Betsuyaku ◽  
Yoshinori Ohtsuka ◽  
...  
Keyword(s):  
Lung Injury ◽  
Migration Inhibitory Factor ◽  
Lung Fibrosis ◽  
Macrophage Migration Inhibitory Factor ◽  
Inhibitory Factor ◽  
Lung Injury Score ◽  
Macrophage Migration ◽  
Acute Lung Inflammation ◽  
Intratracheal Administration

Macrophage migration inhibitory factor (MIF) is a unique cytokine that reportedly overrides the anti-inflammatory effect of endogenous glucocorticoids. MIF has been demonstrated to be involved in a variety of inflammatory diseases. In this study, we examined the role of MIF in bleomycin (BLM)-induced lung injury and fibrosis. The levels of MIF in lung tissues and bronchoalveolar lavage fluids were significantly increased in the period 5–10 days after intratracheal administration of BLM. Treatment with the anti-MIF antibody significantly reduced the mortality at 14 days and the histopathological lung injury score at 10 days. These effects were accompanied with significant suppression of the accumulation of inflammatory cells in the alveolar space and tumor necrosis factor-α in the lungs at 7 days. However, the anti-MIF antibody did not affect either the content of lung hydroxyproline or the histopathological lung fibrosis score at 21 days after BLM. These data provide further evidence for the crucial role of MIF in acute lung inflammation but do not support the involvement of MIF in lung fibrosis induced by BLM in mice.

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