Regulatory role for macrophage migration inhibitory factor in acute respiratory distress syndrome

Donnelly, Seamas C.; Haslett, Chris; Reid, Peter; Grant, I. S.; Wallace, William; Metz, Christine N.; Bruce, Lorna Jacqueline; Bucala, Richard

doi:10.1038/nm0397-320

Cited by 403 publications

(320 citation statements)

References 21 publications

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“…17 MIF is upregulated by TNF-a, and MIF in turn augments the secretion TNF-a. 4,23 Therefore, these inflammatory cytokines may be implicated in the induction or continuation of damage to hair follicles, and MIF may play an important part in the pathophysiology of inflammatory hair loss as in AA. The MIF gene maps to chromosome 22q11.2, and an SNP (G to C transition) in the 5 0 -flanking region at position 173 of the MIF gene is associated with susceptibility to adult inflammatory arthritis.…”

Section: Discussionmentioning

confidence: 99%

Promoter region polymorphism of macrophage migration inhibitory factor is strong risk factor for young onset of extensive alopecia areata

et al. 2005

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We have demonstrated that serum macrophage migration inhibitory factor (MIF) was significantly elevated in patients with extensive alopecia areata (AA). Recently, functional polymorphisms have been identified in the MIF promoter region. To address the functional and prognostic relevance of the À173G/C and À794[CATT] 5-8 repeat polymorphisms in MIF genes in patients with extensive AA, 113 patients with extensive AA and 194 healthy controls were genotyped. We found that MIFÀ173*C was a risk factor for early onset (o20 years) of extensive AA (odds ratio for GC heterozygotes with À173G/C was 4.88 (95% CI, 2.04-11.8), P ¼ 0.00038; odds ratio for CC homozygotes with À173G/C was 10.42 (95% CI, 2.56-43.5), P ¼ 0.0011). We found no statistically significant differences in the genotype frequencies of the À794[CATT] 5-8 repeat polymorphism and extensive AA. These results suggest that polymorphisms within the MIFÀ173*C allele confer an increased risk of susceptibility to the extensive forms of AA, especially with an early onset of disease. MIF is therefore suggested to be closely implicated in the pathogenesis of the more extensive forms of AA.

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Section: Discussionmentioning

confidence: 99%

Promoter region polymorphism of macrophage migration inhibitory factor is strong risk factor for young onset of extensive alopecia areata

et al. 2005

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“…As an important proinflammatory cytokine, MIF can counteract glucocorticoid signaling by activating immune or inflammatory cells and promoting inflammatory cytokine release [9]. Moreover, MIF has been shown to induce various pathologic events, such as acute respiratory distress syndrome [15], arthritis [22], glomerulonephritis [20], and angiogenesis [12,30]. Moreover, Type 1 Modic changes of cartilage end plates are characterized by an inflammatory reaction, but to our knowledge, the relationship between MIF and cartilage end plates with Type 1 Modic changes has not been investigated.…”

Section: Introductionmentioning

confidence: 99%

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

Xiong

Huang

Cun

et al. 2014

Clinical Orthopaedics &Amp; Related Research

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Background Type 1 Modic changes are characterized by edema, vascularization, and inflammation, which lead to intervertebral disc degeneration. Macrophage migration inhibitory factor (MIF) is a proinflammatory cytokine closely related to the inflammatory cytokines detected in degenerative intervertebral disc tissues. However, the existence and role of MIF and its receptor CD74 in intervertebral disc degeneration have not been elucidated. Questions/purposes We asked whether (1) MIF and its receptor CD74 are expressed in cartilage end plates with Type 1 Modic changes, (2) MIF is associated with cartilage end plate degeneration, (3) the MIF antagonist (S, R)-3(4-hydroxyphenyl)-4, 5-dihydro-5-isoxazole acetic acid methyl ester (ISO-1) suppresses MIF-induced inflammatory cytokine release, and (4) inflammatory cytokines are released by cartilage end plate chondrocytes via CD74 by activating the CD74 antibody (CD74Ab). Methods We examined MIF and CD74 expression by human cartilage end plate chondrocytes and tissues with Type 1 Modic changes from eight patients using immunocytofluorescence and immunohistochemistry. MIF production by the chondrocytes was assessed by ELISA and PCR. We compared cytokine release by chondrocytes treated with MIF in the presence or absence of exogenous ISO-1 by ELISA. Cytokine release by chondrocytes after treatment with CD74Ab was determined by ELISA. Results MIF was expressed in degenerated human cartilage end plate tissues and chondrocytes. Lipopolysaccharide and tumor necrosis factor a (TNF-a) upregulated MIF expression and increased MIF secretion in chondrocytes in a dose-dependent manner. MIF increased the secretion of IL-6, IL-8, and prostaglandin E2 (PGE2) in a dose-dependent manner. ISO-1 reduced the secretion of IL-6, IL-8, and PGE2. CD74Ab activated CD74 and induced release of inflammatory cytokines. Conclusions Chondrocytes in cartilage end plate with Type 1 Modic changes express MIF and its receptor CD74.

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“…The cell sources of MIF in asthma likely include resident and recently immigrated cells, specially Th2 lymphocytes and eosinophils. In normal lungs, MIF is constitutively expressed by the bronchial epithelium, alveolar macrophages and capillary endothelium [27,30]. A prominent induction of MIF mRNA and protein has been observed in activated Th2 cells, while eosinophils have pre-formed MIF and are able to secrete high quantities of it upon stimulation [28,31].…”

Section: Introductionmentioning

confidence: 99%

“…By means of antibody neutralization or gene deletion it has been demonstrated that MIF plays an important role in the pathogenesis of several inflammatory disorders, such as sepsis, glomerulonephritis, arthritis, colitis, encephalomyelitis, leishmaniasis and atherosclerosis [11,12,[16][17][18][19][20][21][22][23]. Increased MIF expression has also been observed in patients suffering from inflammatory diseases including sepsis, rheumatoid arthritis, acute respiratory distress syndrome (ARDS) and asthma [11,12,18,[24][25][26][27][28][29]. Bronchoalveolar lavage fluids (BALF), sputum and sera from asthmatic patients were found to contain increased levels of MIF [28,29].…”

Section: Introductionmentioning

confidence: 99%

Macrophage migration inhibitory factor is essential for allergic asthma but not for Th2 differentiation

et al. 2007

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Macrophage migration inhibitory factor (MIF) is increased in asthmatic patients and plays a critical role in the pathogenesis of asthma. We show here that mice lacking MIF failed to develop airway hyper-responsiveness (AHR), tissue eosinophilia, and mucus metaplasia. Analysis of the bronchoalveolar fluids revealed a substantial reduction of IL-13, eotaxin and cysteinyl-leukotrienes. The lack of these cardinal features of asthma in MIF -/-mice occurs regardless of high concentrations of IL-4 in the lung and OVAspecific IgE in the serum. Antigen-specific lymphocyte proliferation and IL-13 production were similarly increased in the draining lymph nodes of OVA-immunized and challenged MIF -/-mice compared to WT, but were reduced in the spleen of MIF -/-, thus indicating differential roles of MIF in these compartments. Stimulation of naive CD4 + cells with anti-CD3 antibody demonstrated that MIF -/-cells produced increased amounts of IFN-c and IL-4 compared to WT CD4 + cells. Finally, treatment of sensitized BALB/c mice with neutralizing anti-MIF antibody abrogated the development of ARH and airway inflammation without affecting the production of Th2 cytokines or IgE. The present study demonstrates that MIF is required for allergic inflammation, adding important elements to our knowledge of asthma pathogenesis and suggesting that neutralization of MIF might be of therapeutic value in asthma. IntroductionAllergic asthma is a disorder characterized by chronic lung inflammation, reversible airway obstruction and increases in airway hyper-responsiveness (AHR) to nonspecific stimuli. Several studies have provided compelling evidences that the lung infiltrating leukocytes and the proinflammatory mediators they produce initiate cellular damage, amplify the immune response, cause airway physiological changes and tissue remodeling [1]. The airway inflammation of asthma has a predominance of Th2 CD4 + lymphocytes, eosinophils and mast cells infiltrating the lung interstitium. Several studies indicate the existence of a mechanism dependent on IL-5 and eosinophils that induce pulmonary damage and intensify AHR [3][4][5]. In other studies, however, the induction of AHR was observed despite the absence of infiltrating eosinophils, suggesting dissociation between these phenomena [6][7][8][9][10]. Macrophage migration inhibitory factor (MIF) is a pleiotropic molecule and critical mediator of innate and acquired immune responses [11,12]. Pre-formed MIF protein is present in many cell types and is released in response to different stimuli, such as infection and cytokine stimulation [12]. MIF exhibits several proinflammatory functions, including the induction of TNF-a, IL-1 and NO release from macrophages, and the production of arachidonic acid and eicosanoids through the induction of phospholipase A 2 and cyclooxygenase [13,14]. A unique property of MIF is its secretion by immune cells in response to physiological increase in glucocorticoid levels. Once released, MIF can counterregulate the anti-inflammatory effects of steroids on cyt...

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Regulatory role for macrophage migration inhibitory factor in acute respiratory distress syndrome

Cited by 403 publications

References 21 publications

Promoter region polymorphism of macrophage migration inhibitory factor is strong risk factor for young onset of extensive alopecia areata

Promoter region polymorphism of macrophage migration inhibitory factor is strong risk factor for young onset of extensive alopecia areata

Migration Inhibitory Factor Enhances Inflammation via CD74 in Cartilage End Plates with Modic Type 1 Changes on MRI

Macrophage migration inhibitory factor is essential for allergic asthma but not for Th2 differentiation

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