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β-Glucan fragmentation by microfluidization and TNF-α-immunostimulating activity of fragmented β-glucans.

ABSTRACT: Fragmentation of β-glucans secreted by the fungus Ophiocordyceps dipterigena BCC 2073 achieved by microfluidization was investigated. The degree of β-glucan fragmentation was evaluated based on the average number of chain scissions (α). The effects on the α value of experimental variables like solid concentration of the β-glucan suspension, interaction chamber pressure, and number of passes through the microfluidizer were examined. Kinetic studies were conducted using the relationships of the α and suspension viscosity values with the number of passes. Evidence indicated that α increases with the interaction chamber pressure and the number of passes, whereas the solid concentration shows the inverted effect. Kinetic data indicated that the fragmentation rate increases with β-glucan solid concentration and interaction chamber pressure. Furthermore, since β-glucan molecular weight is a key factor determining its biological activity, the effect of β-glucans of different molecular weights produced by fragmentation on tumor necrosis factor (TNF)-α-stimulating activity in THP-1 human macrophage cells was investigated. Evidence suggested that β-glucans have an immunostimulating effect on macrophage function, in the absence of cytotoxic effects. Indeed, β-glucans characterized by a range of molecular weights produced via microfluidization exhibited promise as immunostimulatory agents.

SUBMITTER: Nanta P

PROVIDER: S-EPMC11019199 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature

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β-Glucan fragmentation by microfluidization and TNF-α-immunostimulating activity of fragmented β-glucans.

Nanta Phawinee P Buachan Paiwan P Pinket Wichchunee W Srinuanchai Wanwisa W Pongwan Pawinee P Sramala Issara I Jarussophon Suwatchai S Prathumpai Wai W Taweechotipatr Malai M Ruktanonchai Uracha Rungsardthong UR Kasemwong Kittiwut K

Heliyon 20240409 8

Fragmentation of β-glucans secreted by the fungus <i>Ophiocordyceps dipterigena</i> BCC 2073 achieved by microfluidization was investigated. The degree of β-glucan fragmentation was evaluated based on the average number of chain scissions (α). The effects on the α value of experimental variables like solid concentration of the β-glucan suspension, interaction chamber pressure, and number of passes through the microfluidizer were examined. Kinetic studies were conducted using the relationships of ...[more]

PMID: 38628769

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Project description:While Lymphotoxin α (TNF-β), a product of lymphocytes, is known to play a pivotal role in inflammatory joint environment, resveratrol has been shown to possess anti-inflammatory and chondroprotective effects via activation of the histondeacetylase Sirt1. Whether TNF-β induction of inflammatory pathways in primary human chondrocytes (PCH) can be modulated by resveratrol, was investigated. Monolayer and alginate cultures of PCH were treated with TNF-β, anti-TNF-β, nicotinamide (NAM), antisense oligonucleotides against Sirt1 (Sirt1-ASO) and/or resveratrol and co-cultured with T-lymphocytes. We found that resveratrol suppressed, similar to anti-TNF-β, TNF-β-induced increased adhesiveness in an inflammatory microenvironment of T-lymphocytes and PCH. In contrast, knockdown of Sirt1 by mRNA abolished the inhibitory effects of resveratrol on the TNF-β-induced adhesiveness, suggesting the essential role of this enzyme for resveratrol-mediated anti-inflammatory signaling. Similar results were obtained in PCH stimulated with TNF-α. Sirt1-ASO, NAM or TNF-β, similar to T-lymphocytes induced inflammatory microenvironment by down-regulation of cartilage-specific proteins, Sox9, Ki67 and enhanced NF-κB-regulated gene products involved in inflammatory and degradative processes in cartilage (MMP-9/-13, COX-2, caspase-3), NF-κB activation and its translocation to the nucleus. Moreover, resveratrol reversed the TNF-β-, NAM-, T-lymphocytes-induced up-regulation of various NF-κB-regulated gene products. Down-regulation of Sirt1 by mRNA interference abrogated the effect of resveratrol on TNF-β-induced effects. Ultrastructural and cell viability assay investigations revealed that resveratrol revoked TNF-β-induced dose-dependent degradative/apoptotic morphological changes, cell viability and proliferation in PCH. Taken together, suppression of TNF-β-induced inflammatory microenvironment in PCH by resveratrol/Sirt1 might be a novel therapeutic approach for targeting inflammation during rheumatoid arthritis.

Dataset Information

β-Glucan fragmentation by microfluidization and TNF-α-immunostimulating activity of fragmented β-glucans.

Publications

β-Glucan fragmentation by microfluidization and TNF-α-immunostimulating activity of fragmented β-glucans.

Similar Datasets

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