d-pinitol inhibits Th1 polarization via the suppression of dendritic cells

Lee, Jun Sik; Jung, In Duk; Jeong, Young-Il; Lee, Chang-Min; Shin, Yong Kyoo; Lee, Sang‐Yull; Suh, Dong‐Soo; Yoon, Man Soo; Lee, Kyu-Sub; Choi, Yung Hyun; Chung, Hae Young; Park, Yeong‐Min

doi:10.1016/j.intimp.2007.01.018

Cited by 30 publications

(18 citation statements)

References 27 publications

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“…It has been reported that the MAPK and NF-κB pathways, activated by TLR signaling, are involved in the maturation of DCs and the secretion of proinflammatory cytokines (28, 29). In line with these studies, we found that MAB1843 induced the activation of MAPKs and NF-κB in DCs, which is important since DC maturation and proinflammatory cytokine production play a key role in T cell polarization.…”

Section: Discussionsupporting

confidence: 90%

Mycobacterium abscessus ᴅ-alanyl-ᴅ-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity

et al. 2016

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Mycobacterium abscessus, a member of the group of non-tuberculous mycobacteria, has been identified as an emerging pulmonary pathogen in humans. However, little is known about the protective immune response of antigen-presenting cells, such as dendritic cells (DCs), which guard against M. abscessus infection. The M. abscessus gene MAB1843 encodes ᴅ-alanyl-ᴅ-alanine dipeptidase, which catalyzes the hydrolysis of ᴅ-alanyl-ᴅ-alanine dipeptide. We investigated whether MAB1843 is able to interact with DCs to enhance the effectiveness of the host’s immune response. MAB1843 was found to induce DC maturation via toll-like receptor 4 and its downstream signaling pathways, such as the mitogen-activated protein kinase and nuclear factor kappa B pathways. In addition, MAB1843-treated DCs stimulated the proliferation of T cells and promoted Th1 polarization. Our results indicate that MAB1843 could potentially regulate the immune response to M. abscessus, making it important in the development of an effective vaccine against this mycobacterium. [BMB Reports 2016; 49(10): 554-559]

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Section: Discussionsupporting

confidence: 90%

Mycobacterium abscessus ᴅ-alanyl-ᴅ-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity

et al. 2016

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“…In these DC an inhibition of phenotypic maturation and a modulation of cytokine production could be shown, resulting in a significant inhibition of Th1 development. The inhibition of Th1 responses could also be confirmed under in vivo conditions (Lee et al, 2007a).…”

Section: Immunosuppressive Effect Of Acacia Niloticamentioning

confidence: 70%

In vitro and in vivo trypanocidal effect of lipophilic extracts of medicinal plants from Mali and Burkina Faso

Aderbauer

Clausen

Kershaw

et al. 2008

Journal of Ethnopharmacology

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“…Both in vitro and in vivo studies, however, suggest that pinitol is quite safe. For instance, in vitro, pinitol had no cytotoxic effects on normal bone marrow dendritic cells even at 80 Amol/L dose (6). In animal studies, pinitol was found to be quite safe when given at 100 mg/kg (p.o.…”

Section: Discussionmentioning

confidence: 97%

Pinitol targets nuclear factor-κB activation pathway leading to inhibition of gene products associated with proliferation, apoptosis, invasion, and angiogenesis

Sethi

Ahn

Sung

et al. 2008

Molecular Cancer Therapeutics

123

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Pinitol (3-O-methyl-chiroinositol), a component of traditional Ayurvedic medicine (talisapatra), has been shown to exhibit anti-inflammatory and antidiabetic activities through undefined mechanisms. Because the transcription factor nuclear factor-KB (NF-KB) has been linked with inflammatory diseases, including insulin resistance, we hypothesized that pinitol must mediate its effects through modulation of NF-KB activation pathway. We found that pinitol suppressed NF-KB activation induced by inflammatory stimuli and carcinogens. This suppression was not specific to cell type. Besides inducible, pinitol also abrogated constitutive NF-KB activation noted in most tumor cells. The suppression of NF-KB activation by pinitol occurred through inhibition of the activation of IKBA kinase, leading to sequential suppression of IKBA phosphorylation, IKBA degradation, p65 phosphorylation, p65 nuclear translocation, and NF-KB-dependent reporter gene expression. Pinitol also suppressed the NF-KB reporter activity induced by tumor necrosis factor receptor (TNFR)-1, TNFR-associated death domain, TNFR-associated factor-2, transforming growth factor-B -activated kinase-1 (TAK-1)/TAK1-binding protein-1, and IKBA kinase but not that induced by p65. The inhibition of NF-KB activation thereby led to down-regulation of gene products involved in inflammation (cyclooxygenase-2), proliferation (cyclin D1 and c-myc), invasion (matrix metalloproteinase-9), angiogenesis (vascular endothelial growth factor), and cell survival (cIAP1, cIAP2, X-linked inhibitor apoptosis protein, Bcl-2, and Bcl-xL). Suppression of these gene products by pinitol enhanced the apoptosis induced by TNF and chemotherapeutic agents and suppressed TNFinduced cellular invasion. Our results show that pinitol inhibits the NF-KB activation pathway, which may explain its ability to suppress inflammatory cellular responses.

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d-pinitol inhibits Th1 polarization via the suppression of dendritic cells

Cited by 30 publications

References 27 publications

Mycobacterium abscessus ᴅ-alanyl-ᴅ-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity

Mycobacterium abscessus ᴅ-alanyl-ᴅ-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity

In vitro and in vivo trypanocidal effect of lipophilic extracts of medicinal plants from Mali and Burkina Faso

Pinitol targets nuclear factor-κB activation pathway leading to inhibition of gene products associated with proliferation, apoptosis, invasion, and angiogenesis

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