Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin

Murakami, Kohji; Suzuki, Chiaki; Fujii, Akihiro; Imada, Teruaki

doi:10.1007/s00011-012-0452-8

Cited by 5 publications

(3 citation statements)

References 21 publications

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“…It was previously shown that ferritin levels decreased gradually after each plasma exchange session [16]. Furthermore, IVIG may be relevant not only because antibodies against ferritin may be present, but it may also prevent the release of pro-inflammatory cytokines [92]. It is also very interesting to realize that the inhibition of the cytokines that play a central role in AOSD (IL-1 and IL-6) is an effective treatment, since they are the same cytokines known to induce ferritin expression [48].…”

Section: Discussionmentioning

confidence: 99%

“…IVIG probably acts by cytokine- and pathogen-specific antibodies, possibly including antibodies to ferritin [55,91]. Moreover, IVIG prevents the release of pro-inflammatory cytokines in human monocytic cells stimulated with procalcitonin [92]. IVIG is an important modality in the treatment of MAS [93], AOSD [65,76] and cAPS [79,80].…”

Section: Clinical and Laboratory Features In Mas Aosd Caps And Septmentioning

confidence: 99%

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The Hyperferritinemic Syndrome: macrophage activation syndrome, Still’s disease, septic shock and catastrophic antiphospholipid syndrome

Rosário

Zandman‐Goddard

Meyron-Holtz

et al. 2013

BMC Med

416

361

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BackgroundOver the last few years, accumulating data have implicated a role for ferritin as a signaling molecule and direct mediator of the immune system. Hyperferritinemia is associated with a multitude of clinical conditions and with worse prognosis in critically ill patients.DiscussionThere are four uncommon medical conditions characterized by high levels of ferritin, namely the macrophage activation syndrome (MAS), adult onset Still’s disease (AOSD), catastrophic antiphospholipid syndrome (cAPS) and septic shock, that share a similar clinical and laboratory features, and also respond to similar treatments, suggesting a common pathogenic mechanism. Ferritin is known to be a pro-inflammatory mediator inducing expression of pro-inflammatory molecules, yet it has opposing actions as a pro-inflammatory and as an immunosuppressant. We propose that the exceptionally high ferritin levels observed in these uncommon clinical conditions are not just the product of the inflammation but rather may contribute to the development of a cytokine storm.SummaryHere we review and compare four clinical conditions and the role of ferritin as an immunomodulator. We would like to propose including these four conditions under a common syndrome entity termed “Hyperferritinemic Syndrome”.

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Section: Discussionmentioning

confidence: 99%

Section: Clinical and Laboratory Features In Mas Aosd Caps And Septmentioning

confidence: 99%

The Hyperferritinemic Syndrome: macrophage activation syndrome, Still’s disease, septic shock and catastrophic antiphospholipid syndrome

Rosário

Zandman‐Goddard

Meyron-Holtz

et al. 2013

BMC Med

416

361

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“…Many in vitro and in vivo studies have indicated the ability of hIVIG preparations to modulate cytokine induction and release [49-56]. In addition to direct cytokine neutralizing antibodies in hIVIG, there are also other plausible mechanisms [57-59].…”

Section: Discussionmentioning

confidence: 99%

Effects of human intravenous immunoglobulin on amyloid pathology and neuroinflammation in a mouse model of Alzheimer’s disease

Puli

Pomeshchik

Olas

et al. 2012

J Neuroinflammation

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BackgroundHuman intravenous immunoglobulin (hIVIG) preparation is indicated for treating primary immunodeficiency disorders associated with impaired humoral immunity. hIVIG is known for its anti-inflammatory properties and a decent safety profile. Therefore, by virtue of its constituent natural anti-amyloid beta antibodies and anti-inflammatory effects, hIVIG is deemed to mediate beneficial effects to patients of Alzheimer’s disease (AD). Here, we set out to explore the effects of hIVIG in a mouse model of AD.MethodsWe treated APP/PS1dE9 transgenic and wild-type mice with weekly injections of a high hIVIG dose (1 g/kg) or saline for 3 or 8 months. Treatment effect on brain amyloid pathology and microglial reactivity was assessed by ELISA, immunohistochemistry, RT-PCR, and confocal microscopy.ResultsWe found no evidence for reduction in Aβ pathology; instead 8 months of hIVIG treatment significantly increased soluble levels of Aβ40 and Aβ42. In addition, we noticed a significant reduction in CD45 and elevation of Iba-1 markers in specific sub-populations of microglial cells. Long-term hIVIG treatment also resulted in significant suppression of TNF-α and increase in doublecortin positive adult-born neurons in the dentate gyrus.ConclusionsOur data indicate limited ability of hIVIG to impact amyloid burden but shows changes in microglia, pro-inflammatory gene expression, and neurogenic effects. Immunomodulation by hIVIG may account for its beneficial effect in AD patients.

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Intravenous immunoglobulin preparation prevents the production of pro-inflammatory cytokines by modulating NFκB and MAPKs pathways in the human monocytic THP-1 cells stimulated with procalcitonin

Murakami¹,

Suzuki²,

Fujii³

et al. 2014

Inflamm. Res.

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Intravenous immunoglobulin prevents release of proinflammatory cytokines in human monocytic cells stimulated with procalcitonin

Abstract: PCT induced the release of proinflammatory cytokines from THP-1 cells and PBMCs. The function of PCT was prevented by the presence of IVIG.

Cited by 5 publications

References 21 publications

The Hyperferritinemic Syndrome: macrophage activation syndrome, Still’s disease, septic shock and catastrophic antiphospholipid syndrome

The Hyperferritinemic Syndrome: macrophage activation syndrome, Still’s disease, septic shock and catastrophic antiphospholipid syndrome

Effects of human intravenous immunoglobulin on amyloid pathology and neuroinflammation in a mouse model of Alzheimer’s disease

Intravenous immunoglobulin preparation prevents the production of pro-inflammatory cytokines by modulating NFκB and MAPKs pathways in the human monocytic THP-1 cells stimulated with procalcitonin

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