Macrophage migration inhibitory factor has a proinflammatory activity via the p38 pathway in glucocorticoid-resistant ulcerative colitis

Ishiguro, Yoh; Ohkawara, Tatsuya; Sakuraba, Hirotake; Yamagata, Kazufumi; Hiraga, Hiroto; Yamaguchi, Satoko; Fukuda, Shinsaku; Munakata, Akihiro; Nakane, Akio; Nishihira, Jun

doi:10.1016/j.clim.2006.05.010

Cited by 48 publications

(32 citation statements)

References 31 publications

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“…It was also demonstrated that the addition of a steroid-inhibited IL-8 production in the steroid-resistant UC LPMC to a level that was still higher than the spontaneous IL-8 production by control subjects, while the level in responsive cases was suppressed to that of the control subjects. 23 Conversely, the results of the present study showed that the expression levels of MIF in the rectal mucosa of highdosage steroid patients were the same as those of the low-dosage steroid groups. It is hypothesized that MIFrelated changes in the neutrophil profi les of steroidoverdosed UC patients occur even under stable conditions before surgery.…”

Section: Discussioncontrasting

confidence: 63%

Neutrophil dysfunction in steroid-overdosed patients with ulcerative colitis: Potential relevance of macrophage migration inhibitory factor to increased postoperative morbidity

et al. 2011

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Section: Discussioncontrasting

confidence: 63%

Neutrophil dysfunction in steroid-overdosed patients with ulcerative colitis: Potential relevance of macrophage migration inhibitory factor to increased postoperative morbidity

et al. 2011

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“…We have previously shown that CagA is responsible for the induction of gastric epithelial cell production of MIF (5). MIF has been shown to mediate both inflammatory and proliferative responses in many cell types by inducing the NF-B, Erk1/2, and AP-1 signaling pathways (16,26,36). Our studies have also shown that MIF binding to CD74 expressed on the surface of gastric epithelial cells (GECs) led to increased cell proliferation (5).…”

supporting

confidence: 49%

Macrophage Migration Inhibitory Factor and Interleukin-8 Produced by Gastric Epithelial Cells during Helicobacter pylori Exposure Induce Expression and Activation of the Epidermal Growth Factor Receptor

Beswick¹,

Reyes

2008

Infect Immun

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While a link between Helicobacter pylori exposure and gastric cancer has been established, the underlying mechanisms remain unclear. H. pylori induces a chronic inflammatory response in infected individuals. A link between chronic inflammation and carcinogenesis has long been suggested but never elucidated. Epidermal growth factor receptor (EGFR) signaling plays an important role in both proinflammatory and procarcinogenic mechanisms and is upregulated on gastric epithelial cells (GECs) during H. pylori exposure. The aim of this study was to examine the effects of two important proinflammatory cytokines released during H. pylori infection, macrophage migration inhibitory factor (MIF) and interleukin-8 (IL-8), on the expression and transactivation of EGFR and on the proliferation of GECs during H. pylori exposure. The expression of EGFR by GECs was increased by exposure to either H. pylori, recombinant MIF, or recombinant IL-8. However, cag pathogenicity island knockout strains of H. pylori had very little effect on expression. MIF and IL-8 also induced phosphorylation of EGFR, signaling events, and proliferation during H. pylori exposure, all of which were decreased when they were neutralized by these cytokines or were blocked from their receptors. The overall role of EGFR in these responses to H. pylori exposure was assessed by knocking down EGFR expression by small interfering RNA.

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“…MIF signaling seems to be mediated through two distinct pathways -one pathway includes interaction with the intracytoplasmic receptor after its endocytosis while the other pathway is mediated through binding to its surface receptor. Therefore, it could be assumed that MIF differentially induces the signaling cascades in glucocorticoid-resistant and glucocorticoid response patients [Ishiguro et al, 2006].…”

Section: Discussionmentioning

confidence: 99%

Association between Macrophage Migration Inhibitory Factor Gene Variation and Response to Glucocorticoid Treatment in Sudden Sensorineural Hearing Loss

Yazdani¹,

Hamidi

Ghazavi³

et al. 2015

Audiol Neurotol

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Several lines of evidence suggest the role of the immune system in the pathogenesis of sudden sensorineural hearing loss (SSNHL). Macrophage migration inhibitory factor (MIF) mediates its role in various immune and inflammatory conditions by the regulation of immune reactions. Several studies have confirmed an association between MIF gene polymorphisms and susceptibility to various inflammatory and autoimmune disorders. The aim of this study was to explore the association between the MIF (-173 G/C) polymorphism (rs755622) and SSNHL in an Iranian population. In this case-control association study, SSNHL cases (n = 77) were included. Normal healthy subjects (n = 100) were also recruited from the same region. Genotyping for MIF (-173 G/C) polymorphism was carried out using the polymerase chain reaction-restriction fragment length polymorphism technique. The frequency of the MIF -173 C allele carriers (GC + CC genotype) was significantly elevated in SSNHL patients who responded to glucocorticoid treatment compared with the patients with no response to treatment. These results suggest that the MIF gene polymorphism is associated with a response to glucocorticoid treatment in patients with SSNHL.

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Macrophage migration inhibitory factor has a proinflammatory activity via the p38 pathway in glucocorticoid-resistant ulcerative colitis

Cited by 48 publications

References 31 publications

Neutrophil dysfunction in steroid-overdosed patients with ulcerative colitis: Potential relevance of macrophage migration inhibitory factor to increased postoperative morbidity

Neutrophil dysfunction in steroid-overdosed patients with ulcerative colitis: Potential relevance of macrophage migration inhibitory factor to increased postoperative morbidity

Macrophage Migration Inhibitory Factor and Interleukin-8 Produced by Gastric Epithelial Cells during Helicobacter pylori Exposure Induce Expression and Activation of the Epidermal Growth Factor Receptor

Association between Macrophage Migration Inhibitory Factor Gene Variation and Response to Glucocorticoid Treatment in Sudden Sensorineural Hearing Loss

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