Effect of retinoids on LPS-induced COX-2 expression and COX-2 associated PGE2 release from mouse peritoneal macrophages and TNF-α release from rat peripheral blood mononuclear cells

Kim, Bae-Hwan; Kang, Kyung-Sun; Lee, Yong-Soon

doi:10.1016/j.toxlet.2004.01.010

Cited by 67 publications

(38 citation statements)

References 32 publications

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“…This is also consistent with studies showing that RA treatment (38,39) and vitamin A-rich diets (40) can inhibit the development of T1D. Moreover, RA and PGE 2 , an enhancer of Th17 cell development, are reported to be mutually antagonistic, whereby PGE 2 inhibits synthesis of RA and vice versa (41,42).…”

Section: Discussionsupporting

confidence: 89%

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Liu¹,

Lee²,

Sullivan³

et al. 2011

J. Clin. Invest.

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Type 1 diabetes (T1D) is an autoimmune disease that shows familial aggregation in humans and likely has genetic determinants. Disease linkage studies have revealed many susceptibility loci for T1D in mice and humans. The mouse T1D susceptibility locus insulin-dependent diabetes susceptibility 3 (Idd3), which has a homologous genetic interval in humans, encodes cytokine genes Il2 and Il21 and regulates diabetes and other autoimmune diseases; however, the cellular and molecular mechanisms of this regulation are still being elucidated. Here we show that T cells from NOD mice produce more Il21 and less Il2 and exhibit enhanced Th17 cell generation compared with T cells from NOD.Idd3 congenic mice, which carry the protective Idd3 allele from a diabetes-resistant mouse strain. Further, APCs from NOD and NOD.Idd3 mice played a central role in this differential Th17 cell development, and IL-21 signaling in APCs was pivotal to this process. Specifically, NOD-derived APCs showed increased production of pro-Th17 mediators and dysregulation of the retinoic acid (RA) signaling pathway compared with APCs from NOD.Idd3 and NOD.Il21r-deficient mice. These data suggest that the protective effect of the Idd3 locus is due, in part, to differential RA signaling in APCs and that IL-21 likely plays a role in this process. Thus, we believe APCs provide a new candidate for therapeutic intervention in autoimmune diseases.

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Section: Discussionsupporting

confidence: 89%

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Liu¹,

Lee²,

Sullivan³

et al. 2011

J. Clin. Invest.

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“…To date, the suppressive effects of ATRA on cytokine production have been reported in a number of animal diseases. 24,26,27 Recently, Motomura et al 41 and Kim et al 25 have shown the suppressive effects of ATRA on cytokine production induced by macrophages. More recently, we have confirmed that ATRA can suppress hepatic nuclear factor-kB activation, proinflammatory cytokine production and hepatic toxicity induced after the intravenous injection of ATRA-cationic liposome/Luc pDNA complexes.…”

Section: Discussionmentioning

confidence: 99%

“…To date, it is known that ATRA also exerts anti-inflammatory effects by suppressing proinflammatory cytokine production from mesangial cells and macrophages. 24,25 Motomura et al 26 and Osteo et al 27 reported that orally administered ATRA can be used for the treatment of cytokine-induced liver injury and glomerulonephritis in rats. As far as the applications for gene delivery are concerned, suppression of hepatic toxicity mediated by intravenous injection of cationic liposome/pDNA complexes is needed.…”

Section: Introductionmentioning

confidence: 99%

Enhanced growth inhibition of metastatic lung tumors by intravenous injection of ATRA-cationic liposome/IL-12 pDNA complexes in mice

et al. 2010

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Interleukin 12 (IL-12) is a proinflammatory cytokine with antitumor activity. All-trans-retinoic acid (ATRA) exerts antitumor effects by regulating a variety of gene expressions, including tumor necrosis factor receptor 1 (TNFR1), increases the number of TNFR1 and potentiates TNF-a-induced apoptosis in cancer cells. In this study, ATRA-incorporated cationic liposome (ATRA-cationic liposome)/ IL-12 plasmid DNA (pDNA) complexes were prepared to improve therapeutic efficacy of cationic liposome/IL-12 pDNA complexes in a mouse model of metastatic lung tumor after intravenous injection. IL-12 production in lungs by ATRA-cationic liposome/IL-12 pDNA complexes was comparable with that by cationic liposome/IL-12 pDNA complexes. The number of metastatic tumor cells (colon26/Luc) was quantitatively evaluated by measuring luciferase activity. ATRA-cationic liposome/IL-12 pDNA complexes reduced the number of colon26/Luc cells and tumor nodules in lungs. ATRA-cationic liposome/IL-12 pDNA complexes significantly prolonged the survival time of mice, whereas cationic liposome/IL-12 pDNA only slightly prolonged it. ATRA-cationic liposome/IL-12 pDNA complexes increased the TNFR1 mRNA upregulation and the number of apoptotic cells in the lung. Moreover, reduced serum alanine transaminase (ALT) and aspartate transaminase (AST) activities were observed in mice treated with ATRA-cationic liposome/IL-12 pDNA complexes. These results suggest that intravenous injection of ATRA-cationic liposome/IL-12 pDNA complexes is an effective method for the treatment of lung metastasis in mice.

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“…This proinflammatory:antiinflammatory ratio was examined because it is a useful way to represent the balance between such responses and because a previous study reported a marginally significant increase in this ratio as a result of vitamin A supplementation in a human intervention trial using data from whole blood cultures stimulated with a T-cell mitogen (phytohemaglutinin) (12). Whereas these previous data suggest that vitamin A supports production of TNFa, perhaps by supporting the Th1 response, in vitro studies show that retinoic acid suppresses LPS-induced TNFa production in murine macrophages (8,52,53) as well as cord blood mononuclear cells (54). In agreement with these findings, serum TNFa significantly increased after immunization in the low VA group but not in the high VA group, perhaps as a result of stimulation of innate immune cells via toll-like receptors by components of the livevirus YFV vaccine.…”

Section: Discussionmentioning

confidence: 99%

Markers of Innate Immune Function Are Associated with Vitamin A Stores in Men

Ahmad

Haskell

Raqib

et al. 2009

The Journal of Nutrition

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Recommendations for vitamin A intake and liver stores are based on maintaining normal vision. We propose that higher levels may be required to maintain normal innate immune function. To test this hypothesis, we conducted an 8-wk residential study among 36 healthy Bangladeshi men with low vitamin A stores. Subjects were randomized to receive vitamin A (240 mg in 4 doses) or placebo during study wk 2 and 3. They received 2 vaccines during wk 5 and vitamin A stores were estimated by isotopic dilution at wk 8. The serum concentration of the chemokine interferon-g-induced protein 10, a component of T-helper 1 (Th1) response, increased significantly after supplementation and was positively and significantly associated with vitamin A stores. Blood concentrations of natural killer (NK) and NK T-cells, which have anticancer and antiviral activity, were positively associated with stores (P , 0.05), as was monocyte oxidative burst (P , 0.05), a marker of bacterial killing ability. However, serum interleukin (IL)-6 and IL-17, cytokines that regulate the antibacterial Th17 response, were significantly and negatively associated with stores, as was production of the regulatory cytokine IL-10 by whole-blood cultures stimulated with bacterial lipopolysaccharide. In summary, vitamin A stores were positively associated with several measures of innate immune activity across a broad range of stores, suggesting that vitamin A enhances protection against diverse pathogens even at concentrations above those needed to maintain normal vision. The negative association of stores with serum IL-6 and IL-17 suggests that not all protective responses are similarly enhanced by vitamin A.

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Effect of retinoids on LPS-induced COX-2 expression and COX-2 associated PGE2 release from mouse peritoneal macrophages and TNF-α release from rat peripheral blood mononuclear cells

Cited by 67 publications

References 32 publications

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice

Enhanced growth inhibition of metastatic lung tumors by intravenous injection of ATRA-cationic liposome/IL-12 pDNA complexes in mice

Markers of Innate Immune Function Are Associated with Vitamin A Stores in Men

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