MIF: Mood Improving/Inhibiting Factor?

Bloom, Joshua S.; Al‐Abed, Yousef

doi:10.1186/1742-2094-11-11

Cited by 38 publications

(35 citation statements)

References 86 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Indeed, MIF has been shown to promote neuroplasticity and neuroprotective processes under physiological conditions, but it can also increase the production of proinflammatory cytokines under conditions of stress. Moreover, MIF is modulated by glucocorticoids, and high, antiinflammatory doses of glucocorticoids inhibit MIF secretion; however, during pathological conditions characterized by glucocorticoid resistance, such as depression, it is conceivable that levels of MIF are increased (Bloom et al, 2014). In contrast, IL-1β contributes to the activation of other cytokines (IL-18, IL-6) and mediators of oxidative stress, like CASP1, CASP9, and Nitric oxide synthase 2, related to the inflammasome complex, also comprising the Nod-like Receptor, the precursor pro-caspase-1, and the adaptor ASC.…”

Section: Discussionmentioning

confidence: 99%

Absolute Measurements of Macrophage Migration Inhibitory Factor and Interleukin-1-β mRNA Levels Accurately Predict Treatment Response in Depressed Patients

Cattaneo

Ferrari

Uher

et al. 2016

IJNPPY

110

View full text Add to dashboard Cite

Background:Increased levels of inflammation have been associated with a poorer response to antidepressants in several clinical samples, but these findings have had been limited by low reproducibility of biomarker assays across laboratories, difficulty in predicting response probability on an individual basis, and unclear molecular mechanisms.Methods:Here we measured absolute mRNA values (a reliable quantitation of number of molecules) of Macrophage Migration Inhibitory Factor and interleukin-1β in a previously published sample from a randomized controlled trial comparing escitalopram vs nortriptyline (GENDEP) as well as in an independent, naturalistic replication sample. We then used linear discriminant analysis to calculate mRNA values cutoffs that best discriminated between responders and nonresponders after 12 weeks of antidepressants. As Macrophage Migration Inhibitory Factor and interleukin-1β might be involved in different pathways, we constructed a protein-protein interaction network by the Search Tool for the Retrieval of Interacting Genes/Proteins.Results:We identified cutoff values for the absolute mRNA measures that accurately predicted response probability on an individual basis, with positive predictive values and specificity for nonresponders of 100% in both samples (negative predictive value=82% to 85%, sensitivity=52% to 61%). Using network analysis, we identified different clusters of targets for these 2 cytokines, with Macrophage Migration Inhibitory Factor interacting predominantly with pathways involved in neurogenesis, neuroplasticity, and cell proliferation, and interleukin-1β interacting predominantly with pathways involved in the inflammasome complex, oxidative stress, and neurodegeneration.Conclusion:We believe that these data provide a clinically suitable approach to the personalization of antidepressant therapy: patients who have absolute mRNA values above the suggested cutoffs could be directed toward earlier access to more assertive antidepressant strategies, including the addition of other antidepressants or antiinflammatory drugs.

show abstract

Section: Discussionmentioning

confidence: 99%

Absolute Measurements of Macrophage Migration Inhibitory Factor and Interleukin-1-β mRNA Levels Accurately Predict Treatment Response in Depressed Patients

Cattaneo

Ferrari

Uher

et al. 2016

IJNPPY

110

View full text Add to dashboard Cite

show abstract

“…There has been increasing interest in the role of the pro-inflammatory protein M migration inhibitory factor (MIF) in depression and TB. 94,95 MIF is an important regulator of innate immunity that is secreted primarily by M s and T cells. 96 This factor inhibits M migration and promotes the gathering, infiltration, and proliferation of M s at inflammatory sites.…”

Section: Migration Inhibitory Factormentioning

confidence: 99%

The interplay between depression and tuberculosis

Zhang

Wang

et al. 2019

Journal of Leukocyte Biology

View full text Add to dashboard Cite

Depression is a major mental health condition and is expected be the most debilitating and widespread health disorder by 2030. Tuberculosis (TB) is also a leading cause of morbidity and mortality worldwide and interestingly, is a common comorbidity of depression. As such, much attention has been paid to the association between these 2 pathologies. Based on clinical reports, the association between TB and depression seems to be bidirectional, with a substantial overlap in symptoms between the 2 conditions. TB infection or reactivation may precipitate depression, likely as a consequence of the host's inflammatory response and/or dysregulation of the hypothalamic–pituitary–adrenal axis. Nevertheless, few studies have considered whether patients with depression are at a higher risk for TB. In this review, we discuss the hypotheses on the association between depression and TB, highlighting the immuno‐inflammatory response and lipid metabolism as potential mechanisms. Improving our understanding of the interplay between these 2 disorders should help guide TB clinical care and prevention both in patients with comorbid depression and in the general population.

show abstract

“…Depressed patients show evidence of impaired neuroplasticity and antidepressant medications enhance neuroplasticity at both the molecular and the cellular level [9]. There is also an inflammatory hypothesis of depression, which is proposed by the observation that elevated levels of proinflammatory cytokines are present both in blood plasma, and in the cerebrospinal fluid during depressive states in patients [10,11].…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

“…Macrophage migration inhibitory factor is a proinflammatory cytokine, with functions in inflammation, apoptosis, metabolic and neuroendocrine processes [64]. This protein can be linked to depression as part of the inflammatory hypothesis of the disease, which comes from the finding that in depressive states, elevated levels of proinflammatory cytokines can be measured both in the plasma and cerebrospinal fluid [10,11], and that anti-inflammatory treatments can exert antidepressant effect [65]. Interestingly, others also associated MIF level alterations with depressive and anxiety symptoms [66][67][68].…”

Section: Mif Hypothalamic-pituitary-adrenal Axis and Inflammationmentioning

confidence: 99%