Variations in macrophage migration inhibitory factor gene are not associated with visceral leishmaniasis in India

Mishra, Anshuman; Sundaravadivel, Pandarisamy; Tripathi, Sunil Kumar; Jha, Rajan Kumar; Badrukhiya, Jaydeep; Basak, Nipa; Anerao, Isha; Sharma, Akshay; Ajayi, Ebenezer Idowu O; Mishra, Abhishek; Pandey, SS; Kumar, Umesh; Singh, Sakshi; Nizamuddin, Sheikh; Tupperwar, Nitin; Jha, Aditya Nath; Thangaraj, Kumarasamy

doi:10.1016/j.jiph.2018.12.011

Cited by 4 publications

(2 citation statements)

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“…While the impact of host MIF on experimental L. major infection in mice has been well characterized, the impact of the cytokine in human leishmaniasis is less well understood. In one study, it was reported that the -173C single-nucleotide promoter polymorphism that is in linkage disequilibrium with the high expression MIF CATT-7 allele was associated with increased cutaneous disease severity in patients from Brazil infected with L. braziliensis, while in a separate study no difference in visceral leishmaniasis disease severity was observed in Indian individuals infected with L. donovani with differing MIF gene variants [97,98]. Another study found that plasma MIF and lipopolysaccharide levels were elevated in patients with American visceral leishmaniasis co-infected with HIV, and corresponded with a weakened T cell response and worsened systemic inflammation [99].…”

Section: Role Of Host Mif During Leishmaniasismentioning

confidence: 98%

Role of Host and Parasite MIF Cytokines during Leishmania Infection

Holowka

Bucala

2020

TropicalMed

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Macrophage migration inhibitory factor (MIF) is an immunoregulatory cytokine that has been extensively characterized in human disease and in mouse models. Its pro-inflammatory functions in mammals includes the retention of tissue macrophages and a unique ability to counteract the immunosuppressive activity of glucocorticoids. MIF also acts as a survival factor by preventing activation-induced apoptosis and by promoting sustained expression of inflammatory factors such as TNF-α and nitric oxide. The pro-inflammatory activity of MIF has been shown to be protective against Leishmania major infection in mouse models of cutaneous disease, however the precise role of this cytokine in human infections is less clear. Moreover, various species of Leishmania produce their own MIF orthologs, and there is evidence that these may drive an inflammatory environment that is detrimental to the host response. Herein the immune response to Leishmania in mouse models and humans will be reviewed, and the properties and activities of mammalian and Leishmania MIF will be integrated into the current understandings in this field. Furthermore, the prospect of targeting Leishmania MIF for therapeutic purposes will be discussed.

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Section: Role Of Host Mif During Leishmaniasismentioning

confidence: 98%

Role of Host and Parasite MIF Cytokines during Leishmania Infection

Holowka

Bucala

2020

TropicalMed

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“…MIF is a regulator with multiple immune effects, which can regulate the transcription of target genes through the activation of downstream molecules by phosphorylation and participate in a series of pathophysiological processes such as cell growth and migration and inflammation and immune response regulation. There is a lot of evidence that parasite-derived MIF is similar in structure and function to human-derived MIF, affecting macrophage polarization and immune evasion ( 2 , 3 ).…”

Section: Introductionmentioning

confidence: 99%

Dynamic changes in human THP-1-derived M1-to-M2 macrophage polarization during Thelazia callipaeda MIF induction

Yin

Cai²,

Gou³

et al. 2023

Front. Immunol.

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Macrophages are innate immune cells with essential roles in the immune response during helminth infection. Particularly, the direction of macrophage polarization could contribute to pathogen trapping and killing as well as tissue repair and the resolution of type 2 inflammation. This study establishes that the recombinant protein of Thelazia callipaeda macrophage migration inhibitory factor (T.cp-MIF) induces THP-1-derived macrophages to undergo M1 to M2 type dynamic polarization, using the methods of flow cytometry, real-time quantitative PCR, differential transcriptomic analysis and western blot. Interestingly, there was an increase in protein and mRNA expression of M1-type proteins and cytokines after the use of PI3K inhibitors, suggesting that the polarization state tends to favor the M1 type after M2 type inhibition. In conclusion, the dynamic polarization mechanism of T.cp-MIF-induced human THP-1-derived macrophages from M1 to M2 type is related to the binding of TLR4. It can first affect the M1 type polarization of macrophages by activating its downstream NF-κB pathway. Activation of the PI3K/Akt pathway and inhibition of NF-κB phosphorylation affects the M2 type polarization of macrophages.

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