Soluble Glucan Is Internalized and Trafficked to the Golgi Apparatus in Macrophages via a Clathrin-Mediated, Lipid Raft-Regulated Mechanism

Ozment, Tammy R.; Goldman, Matthew P.; Kalbfleisch, John H.; Williams, David L.

doi:10.1124/jpet.112.196329

Cited by 14 publications

(10 citation statements)

References 36 publications

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“…Dectin-1 a C-type lectin receptor, which recognizes the glucans of the fungal cell wall[128] gets concentrated in lipid rafts upon stimulation with glucans[129]. In fact, disruption of lipid rafts by means of cholesterol extraction leads to a reduction in glucan uptake[129,130]. Furthermore, various fungal pathogens such as C. neoformans and P. brasiliensis bind to monosialotetrahexosylganglioside (GM1)[131,132], a component of mammalian lipid rafts[133], or associate with GM1 localized areas during infection[134].…”

Section: Membrane Microdomains and Virulencementioning

confidence: 99%

Plasma membrane lipids and their role in fungal virulence

Rella

Farnoud

Poeta

2016

Progress in Lipid Research

104

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There has been considerable evidence in recent years suggesting that plasma membrane lipids are important regulators of fungal pathogenicity. Various glycolipids have been shown to impart virulent properties in several fungal species, while others have been shown to play a role in host defense. In addition to their role as virulence factors, lipids also contribute to other virulence mechanisms such as drug resistance, biofilm formation, and release of extracellular vesicles. In addition, lipids also affect the mechanical properties of the plasma membrane through the formation of packed microdomains composed mainly of sphingolipids and sterols. Changes in the composition of lipid microdomains has been shown to disrupt the localization of virulence factors and affect fungal pathogenicity. This review gathers evidence on the various roles of plasma membrane lipids in fungal virulence and how lipids might contribute to the different processes that occur during infection and treatment. Insight into the role of lipids in fungal virulence can lead to an improved understanding of the process of fungal pathogenesis and the development of new lipid-mediated therapeutic strategies.

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Section: Membrane Microdomains and Virulencementioning

confidence: 99%

Plasma membrane lipids and their role in fungal virulence

Rella

Farnoud

Poeta

2016

Progress in Lipid Research

104

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“…This also suggests that the immune regulation of COS6 on macrophages is closely related to lipid rafts. After COS6 is internalized with MR CTLD4-8, it may be sent to the lysosome ( 51 ) or through the endosome to the Golgi apparatus ( 52 ), and the ligand is degraded after separation, to fully exert the immune regulatory effect of COS6.…”

Section: Discussionmentioning

confidence: 99%

Mannose Receptor Mediates the Activation of Chitooligosaccharides on Blunt Snout Bream (Megalobrama amblycephala) Macrophages

Ouyang

Wang

et al. 2021

Front. Immunol.

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Chitooligosaccharide (COS) is an important immune enhancer and has been proven to have a variety of biological activities. Our previous research has established an M1 polarization mode by COS in blunt snout bream (Megalobrama amblycephala) macrophages, but the mechanism of COS activation of blunt snout bream macrophages remains unclear. In this study, we further explored the internalization mechanism and signal transduction pathway of chitooligosaccharide hexamer (COS6) in blunt snout bream macrophages. The results showed that mannose receptor C-type lectin-like domain 4-8 of M. amblycephala (MaMR CTLD4-8) could recognize and bind to COS6 and mediate COS6 into macrophages by both clathrin-dependent and caveolin-dependent pathways. In the inflammatory response of macrophages activated by COS6, the gene expression of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and nitric oxide synthase 2 (NOS2) was significantly inhibited after MaMR CTLD4-8-specific antibody blockade. However, even if it was blocked, the expression of these inflammation-related genes was still relatively upregulated, which suggested that there are other receptors involved in immune regulation. Further studies indicated that MaMR CTLD4-8 and Toll-like receptor 4 (TLR4) cooperated to regulate the pro-inflammatory response of macrophages caused by COS6. Taken together, these results revealed that mannose receptor (MR) CTLD4-8 is indispensable in the process of recognition, binding, internalization, and immunoregulation of COS in macrophages of blunt snout bream.

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“…The reason for these variable induction activities of TRAIL mRNA after stimulation with AP-PG is unknown. The significance of phagocytosis-mediated cell internalization on the recognition of β-glucans followed by activation of immune response was reported in other organism-derived β-glucans [ 31 ]. As similar with other organism-derived β-glucans, internalization of AP-PG into the cell is thought to be important for activation of signaling pathway required for TRAIL induction.…”

Section: Discussionmentioning

confidence: 99%

Stimulation of Macrophages with the β-Glucan Produced by Aureobasidium pullulans Promotes the Secretion of Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL)

et al. 2015

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A β-glucan produced by Aureobasidium pullulans (AP-PG) is consisting of a β-(1,3)-linked main chain with β-(1,6)-linked glucose side residues. Various β-glucans consisting of β-(1,3)-linked main chain including AP-PG are believed to exhibit anti-tumor activities, and actually, anti-tumor activities of AP-PG in mice have been demonstrated. In this study, we demonstrate that stimulation with AP-PG induces TRAIL expression in mouse and human macrophage-like cell lines. TRAIL is known to be a cytokine which specifically induces apoptosis in transformed cells, but not in untransformed cells. The expression of TRAIL mRNA after stimulation with AP-PG was increased in RAW264.7 cells, Mono Mac 6 cells, and macrophage-differentiated THP-1 cells. The mRNA expression of TNF-α and FasL is only weakly increased after stimulation with AP-PG. The induction activity of TRAIL by curdlan, a bacterial β-glucan, was very similar to that by AP-PG in RAW264.7 cells, but weaker in macrophage-differentiated THP-1 cells. Activation of caspases was found in HeLa cells after treatment with the supernatant of cultured medium from AP-PG-stimulated Mono Mac 6 cells, and was inhibited by the anti-TRAIL neutralizing antibody. These findings suggest that the stimulation with AP-PG effectively induces TRAIL in macrophages, and that it may be related to apoptosis induction of tumor cells.

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Soluble Glucan Is Internalized and Trafficked to the Golgi Apparatus in Macrophages via a Clathrin-Mediated, Lipid Raft-Regulated Mechanism

Cited by 14 publications

References 36 publications

Plasma membrane lipids and their role in fungal virulence

Plasma membrane lipids and their role in fungal virulence

Mannose Receptor Mediates the Activation of Chitooligosaccharides on Blunt Snout Bream (Megalobrama amblycephala) Macrophages

Stimulation of Macrophages with the β-Glucan Produced by Aureobasidium pullulans Promotes the Secretion of Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL)

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