Particulate β‐glucans synergistically activate TLR4 and Dectin‐1 in human dendritic cells

Sahasrabudhe, Neha M.; Dokter-Fokkens, Jelleke; Vos, Paul de

doi:10.1002/mnfr.201600356

Cited by 54 publications

(43 citation statements)

References 42 publications

(66 reference statements)

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“…In this study, we found that NF-κB was markedly activated after LPS exposure in the lung ( p < 0.05) (Table 6). As the upstream signal of NF-κB [11, 12], TLR4 and Myd88 were also determined and the results showed that LPS upregulated expression of TLR4 and Myd88 in the lung ( p < 0.05). Meanwhile, indirubin markedly inhibited TLR4 and NF-κB signals, which might further mediate the oxidative stress and inflammation in the LPS-induced acute lung injury.…”

Section: Resultsmentioning

confidence: 99%

Indirubin improves antioxidant and anti-inflammatory functions in lipopolysaccharide-challenged mice

2017

Oncotarget

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Indirubin, a traditional Chinese medicine formulation from the Muricidae family, has been reported to exhibit abroad anti-cancer and anti-inflammation activities and mediate nuclear factor-κB (NF-κB) signal. Thus, this study aimed to investigate the protective effects of indirubin on LPS-induced acute lung injury and the potential mechanism in mice. The results showed that LPS treatment caused oxidative stress and inflammation in mice. Indirubin alleviated LPS-caused oxidative stress and inflammation via reducing MDA abundance and IL-1β and TNF-α expressions in mice. Meanwhile, indirubin improved lung NO production and inhibited NF-κB activation caused by LPS exposure. In conclusion, indirubin alleviated LPS-induced acute lung injury via improving antioxidant and anti-inflammatory functions, which might be associated with the NO and NF-κB signals.

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Section: Resultsmentioning

confidence: 99%

Indirubin improves antioxidant and anti-inflammatory functions in lipopolysaccharide-challenged mice

2017

Oncotarget

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“…Fungal ␤-GPs are primarily recognized by the C-type lectin receptor Dectin-1, which is expressed in both immune cells, such as monocytes and macrophages (36,37), and nonimmune cells, such as human bronchial epithelial and intestinal epithelial cells (38,39). Dectin-1 recognizes ␤-glucan, which promotes antifungal effector mechanisms and production of inflammatory mediators (39), and in some cases cooperates with TLR2 and TLR4 to mediate this response (40,41). Although the function of Dectin-1 and its expression in the oral epithelium are still unknown (42), we detected its expression in RT7 keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

Candida albicans β-Glucan-Containing Particles Increase HO-1 Expression in Oral Keratinocytes via a Reactive Oxygen Species/p38 Mitogen-Activated Protein Kinase/Nrf2 Pathway

et al. 2018

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Oral keratinocytes provide the first line of host defense against oral candidiasis. We speculated that interactions of fungal cell wall components with oral keratinocytes regulate the stress response against infection and examined the expression of genes induced by heat-killed in oral immortalized keratinocytes using a cDNA microarray technique. Of 24,000 genes revealed by that analysis, we focused on HO-1, a stress-inducible gene, as its expression was increased by both heat-killed and live In histological findings, HO-1 expression in the superficial layers of the oral epithelium following infection was elevated compared to that in healthy epithelium. We then investigated fungal cell wall components involved in induction of HO-1 expression and found that β-glucan-containing particles (β-GPs) increased its expression. Furthermore, β-glucan was observed on the surface of both heat-killed and cells that had invaded the oral epithelium. Fungal β-GPs also promoted induction of intracellular reactive oxygen species (ROS), NADPH oxidase activation, and p38 mitogen-activated protein kinase (MAPK) phosphorylation, while those specific inhibitors inhibited the HO-1 expression induced by fungal β-GPs. Moreover, fungal β-GPs induced Nrf2 translocation into nuclei via p38 MAPK signaling, while the HO-1 expression induced by fungal β-GPs was inhibited by Nrf2-specific small interfering RNA (siRNA). Finally, knockdown of cells by HO-1- and Nrf2-specific siRNAs resulted in increased β-GP-mediated ROS production compared to that in the control cells. Our results show that the HO-1 induced by fungal β-GPs via ROS/p38 MAPK/Nrf2 from oral keratinocytes may have important roles in host defense against the stress caused by infection in the oral epithelium.

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“…However, lemon pectin with low DM blocked TLR2/1 instead of activating the receptor 6 . In human dendritic cells, β-glucans synergistically activate TLR4 and Dectin-1 32 . β2 → 1-fructans activated TLR2, while TLR4, 5, 7 and 8 were mildly activated in reporter HEK cells 14 .…”

Section: Discussionmentioning

confidence: 99%

Pectin Interaction with Immune Receptors is Modulated by Ripening Process in Papayas

Prado

Beukema

Jermendi

et al. 2020

Sci Rep

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Dietary fibers have been shown to exert immune effects via interaction with pattern recognition receptors (pRR) such as toll-like receptors (tLR) and nucleotide-binding oligomerization domain (noD)like receptors. Pectin is a dietary fiber that interacts with PRR depending on its chemical structure. Papaya pectin retains different chemical structures at different ripening stages. How this influence PRR signaling is unknown. The aim of this work was to determine how ripening influences pectin structures and their ability to interact with TLR2, 3, 4, 5 and 9, and NOD1 and 2. It was evaluated the interaction of the water-soluble fractions rich in pectin extracted from unripe to ripe papayas. The pectin extracted from ripe papayas activated all the TLR and, to a lesser extent, the NOD receptors. The pectin extracted from unripe papayas also activated TLR2, 4 and 5 but inhibited the activation of TLR3 and 9. The differences in pectin structures are the higher methyl esterification and smaller galacturonan chains of pectin from ripe papayas. Our finding might lead to selection of ripening stages for tailored modulation of pRR to support or attenuate immunity. Dietary fibers (DF) commonly represent a wide variety of polysaccharides originating from fruits, vegetables, whole grains and legumes with several health benefits. Such benefits include slow gastric empty 1 and improve physical bowel function 2. Besides the physical benefits, DF can also interact directly with intestinal cells and/or the immune cells from the mucosa 3-5. It is not just the direct effects of DF on cells may trigger immune modulations 6 but also the DF fermentation in the gut 7,8. The direct interaction of DF with the intestinal cells may occur through pattern recognition receptors (PRR) 9. The PRR are germline-encoded sensors expressed in intestinal epithelial cells and gut immune cells. PRR are the key receptors responsible for the recognition of exogenous molecules by the host 5,9. Toll-like receptors (TLR) are a family of PRR that play a central role in the activation of innate immunity 10 and have been shown to be involved in DF-induced immune signaling as described below. The immune response mediated by TLR activation requires the recruitment of myeloid differentiation primary response protein 88 (MyD88) adaptor and the translocation of NF-κB to the nucleus 10. Only TLR3 NF-κB activation is not dependent on MyD88 protein which is mediated by TIR domain-containing adapter inducing IFN-β (TRIF), though 11. The interactions between wide variety of DF and TLR have been extensively studied. DF have a complex and heterogeneous structure and some DF activate TLR to different extents 12 while other DF (such as pectin) seem to block TLR signaling and attenuate intestinal inflammation 6. Nucleotide-binding oligomerization domains (NOD) have also been shown to be influenced by DF, such as β2 → 1-fructans. NOD are proteins responsible for the recognition of intracellular bacteria 10. Through this signaling via PRR, DF have been shown to mediate several ho...

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Particulate β‐glucans synergistically activate TLR4 and Dectin‐1 in human dendritic cells

Abstract: These results suggest that TLR4 and Dectin-1 are synergistically activated by particulate β-glucans, wherein TLR4 activates an immune regulatory pathway in human dendritic cells. Our data suggest that β-glucan is an immune regulatory ligand for TLR4.

Cited by 54 publications

References 42 publications

Indirubin improves antioxidant and anti-inflammatory functions in lipopolysaccharide-challenged mice

Indirubin improves antioxidant and anti-inflammatory functions in lipopolysaccharide-challenged mice

Candida albicans β-Glucan-Containing Particles Increase HO-1 Expression in Oral Keratinocytes via a Reactive Oxygen Species/p38 Mitogen-Activated Protein Kinase/Nrf2 Pathway

Pectin Interaction with Immune Receptors is Modulated by Ripening Process in Papayas

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