Modulation of muramyl dipeptide stimulation of cytokine production by blood components

Meer, Jonathan H M van der; Netea, M.G.; Dinarello, Charles A.

doi:10.1111/j.1365-2249.2009.03926.x

Cited by 15 publications

(14 citation statements)

References 24 publications

(28 reference statements)

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“…This would mean that the highest dilution of pustulan in the WBA (25μg/ml) - which still gave strong cytokine responses - contained maximally 45 ng/ml PGN. Rockel et al 33 reported that PGN alone does not stimulate a cytokine response in human whole blood at 10 μg/ml, and van der Meer et al 34 found the same result for muramyldipeptide in human whole blood. Thus the concentration of PGN measured in our glucan preparations was clearly below the minimum level required for cytokine induction.…”

Section: Discussionmentioning

confidence: 88%

Comparison of the potency of a variety of β-glucans to induce cytokine production in human whole blood

et al. 2012

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Beta-glucans are components of fungal cell walls and potent stimulants of innate immunity. The majority of research on biological activities of glucans has focused on β-(1,3)-glucans, which have been implicated in relation with fungal exposure-associated respiratory symptoms, and as important stimulatory agents in anti-fungal immune responses. Fungi - and bacteria and plants - produce a wide variety of glucans with vast differences in proportion and arrangement of their 1,3-, 1,4-, and 1,6-β-glycosidic linkages. Thus far the proinflammatory potential of different β-glucans has not been studied within the same experimental model. Therefore, we compared the potency of 13 different glucan preparations to induce in vitro production of IL1β, IL6, IL8 and TNF-α in human whole blood cultures. The strongest inducers of all cytokines were pustulan (β-(1,6)-glucan), lichenan (β-(1,3)-(1,4)-glucan), xyloglucan (β-(1,4)-glucan), and pullulan (α-(1,4)-(1,6)-glucan). Moderate to strong cytokine production was observed for curdlan (β-(1,3)-glucan), baker’s yeast glucan (β-(1,3)-(1,6)-glucan), and barley glucan (β-(1,3)-(1,4)-glucan), while all other glucan preparations induced only low or no detectable levels of cytokines. We therefore conclude that innate immunity reactions are not exclusively induced by β-(1,3)-glucans, but also by β-(1,6)- and β-(1,4)-structures. Thus, not only β-(1,3)-glucan, but also other β-glucans and particularly β-(1,6)-glucans should be considered in future research.

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Section: Discussionmentioning

confidence: 88%

Comparison of the potency of a variety of β-glucans to induce cytokine production in human whole blood

et al. 2012

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“…Similarly to Candida stimulation, LPSinduced IL-1b and TNF-a production by PBMCs was lowered in the presence of PMNs (Fig. 1B) (21). To investigate whether the decreased cytokine concentration could be explained by internalization of the cytokine in the cell or by binding of the cytokine to membrane-bound receptors, we measured the concentration of TNF in the cells lysed in Triton-X, which represents the concentration of intracellular and membrane-bound TNF.…”

Section: Resultsmentioning

confidence: 93%

“…Recently, we made the observation that neutrophils modulate cytokine production stimulated by bacterial peptidoglycans and LPS (21). As both neutrophils and proinflammatory cytokines are essential in host defense against C. albicans, we investigated whether neutrophils could also modulate cytokines produced by PBMCs after stimulation with Candida.…”

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confidence: 99%

Neutrophil-Mediated Inhibition of Proinflammatory Cytokine Responses

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et al. 2012

The Journal of Immunology

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Neutrophils (polymorphonuclear neutrophils [PMNs]) play an elaborate role in the innate immune response against invading pathogens. Recent research provided evidence that PMNs can play a modulatory role in inflammation next to their primary role of phagocytosis. In the current study, we investigated whether neutrophils can modulate the innate immune response against Candida albicans. Production of the proinflammatory cytokines IL-1β and TNF-α by human PBMCs in response to C. albicans or LPS was decreased by coculture of PMNs; however, the anti-inflammatory cytokine IL-10 remained unaffected. Using Transwells and cells of patients with chronic granulomatous disease, we show that this downregulation of proinflammatory cytokine production was independent of phagocytosis and reactive oxygen species but was dependent on a soluble factor. We suggest that neutrophil-derived proteases are responsible for the downregulation of IL-1β and TNF-α, as cytokine production could be recovered by addition of α1-antitrypsin, an endogenous inhibitor of serine proteases. PMN lysates and neutrophil elastase could degrade recombinant human IL-1β and TNF-α but not IL-10, and this could be inhibited by addition of α1-antitrypsin. Moreover, we also provide evidence that the dampening effect of PMNs is present in vivo in a murine zymosan-induced arthritis model and a murine experimental endotoxemia model. Altogether, our data show that PMNs can dampen the proinflammatory response to C. albicans by protease-mediated degradation of cytokines. This observation suggest that PMNs might play a important regulatory role in the host defense against C. albicans and can be important for understanding the regulation of inflammation in general.

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“…For instance, neutrophils release proteases that not only degrade extracellular matrices and cells surrounding the inflammatory milieu but also deactivate inflammatory cytokines ( 180 ). Additionally, neutrophils modulate the cytokine production stimulated by bacterial peptidoglycans and LPS ( 181 ). In vitro studies have shown that PMN lysates and neutrophil elastase can degrade recombinant human IL-1β and TNF-α but not IL-10, and alpha1-antitrypsin can inhibit this process ( 180 ).…”

Section: How Does Resolution Start?mentioning

confidence: 99%

Resolution of Inflammation: What Controls Its Onset?

et al. 2016

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An effective resolution program may be able to prevent the progression from non-resolving acute inflammation to persistent chronic inflammation. It has now become evident that coordinated resolution programs initiate shortly after inflammatory responses begin. In this context, several mechanisms provide the fine-tuning of inflammation and create a favorable environment for the resolution phase to take place and for homeostasis to return. In this review, we focus on the events required for an effective transition from the proinflammatory phase to the onset and establishment of resolution. We suggest that several mediators that promote the inflammatory phase of inflammation can simultaneously initiate a program for active resolution. Indeed, several events enact a decrease in the local chemokine concentration, a reduction which is essential to inhibit further infiltration of neutrophils into the tissue. Interestingly, although neutrophils are cells that characteristically participate in the active phase of inflammation, they also contribute to the onset of resolution. Further understanding of the molecular mechanisms that initiate resolution may be instrumental to develop pro-resolution strategies to treat complex chronic inflammatory diseases, in humans. The efforts to develop strategies based on resolution of inflammation have shaped a new area of pharmacology referred to as “resolution pharmacology.”

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Modulation of muramyl dipeptide stimulation of cytokine production by blood components

Cited by 15 publications

References 24 publications

Comparison of the potency of a variety of β-glucans to induce cytokine production in human whole blood

Comparison of the potency of a variety of β-glucans to induce cytokine production in human whole blood

Neutrophil-Mediated Inhibition of Proinflammatory Cytokine Responses

Resolution of Inflammation: What Controls Its Onset?

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