Lipopolysaccharide (LPS)-induced Interferon (IFN)-gamma Production by Decidual Mononuclear Cells (DMNC) is Interleukin (IL)-2 and IL-12 Dependent

Negishi, Masami; Izumi, Yasushi; Sheikh, Aleemuzzaman; Inaba, Noriyuki; Hayakawa, Satoshi

doi:10.1111/j.1600-0897.2010.00856.x

Cited by 15 publications

(21 citation statements)

References 41 publications

(41 reference statements)

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“…Consistent with this observation, we also found Ber promoted IL-12 p40 production in LPS-challenged mice, which was inhibited by Y. It has been demonstrated that IL-12 upregulates IFN-γ regulation [25]. Thus, in this study, increased IFN-γ production by Ber in LPS-challenged mice may be related with enhanced IL-12 production, but the mechanism by which Ber plus Y promoted IFN-γ production in endotoxemic mice needs to be further investigated.…”

Section: Discussionsupporting

confidence: 91%

Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms

Wang

Zhang

et al. 2012

PLoS ONE

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Sepsis remains a major cause of mortality in intensive care units, better therapies are urgently needed. Gram-negative bacterial lipopolysaccharide (LPS) is an important trigger of sepsis. We have demonstrated that berberine (Ber) protects against lethality induced by LPS, which is enhanced by yohimbine (Y) pretreatment, and Ber combined with Y also improves survival in septic mice. However, the precise mechanisms by which Y enhances protection of Ber against LPS - induced lethality remain unclear. The present study confirmed that simultaneously administered Y also enhanced protection of Ber against LPS-induced lethality. Ber or/and Y attenuated liver injury, but not renal injury in LPS-challenged mice. Ber or/and Y all inhibited LPS-stimulated IκBα, JNK and ERK phosphorylation, NF-κB activation as well as TNF-α production. Ber also increased IL-10 production in LPS-challenged mice, which was enhanced by Y. Furthermore, Ber or/and Y all suppressed LPS-induced IRF3, TyK2 and STAT1 phosphorylation, as well as IFN-β and IP-10 mRNA expression in spleen of mice at 1 h after LPS challenge. Especially, Y enhanced the inhibitory effect of Ber on LPS-induced IP-10 mRNA expression. In vitro experiments further demonstrated that Y significantly enhanced the inhibitory effect of Ber on TNF-α production in LPS-treated peritoneal macrophages, Ber combined with Y promoted LPS-induced IL-10 production and LPS-stimulated IκBα, JNK, ERK and IRF3 phosphorylation and NF-κB activation were also suppressed by Ber or/and Y pretreatment in peritoneal macrophages. Taken together, these results demonstrate that Y enhances the protection of Ber against LPS-induced lethality in mice via attenuating liver injury, upregulating IL-10 production and suppressing IκBα, JNK, ERK and IRF3 phosphorylation. Ber combined with Y may be an effective immunomodulator agent for the prevention of sepsis.

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Section: Discussionsupporting

confidence: 91%

Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms

Wang

Zhang

et al. 2012

PLoS ONE

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“…Studies have shown that IFNγ plays a deciding role in whether immune cells attack and injure the CNS, and that LPS stimulates IFNγ production in immune cells3132. We thus questioned whether GA could reduce the phosphorylation of STAT1 and −3 via affecting the production of IFNγ or the activation of IFNγ receptor (IFNγR).…”

Section: Resultsmentioning

confidence: 99%

Glatiramer acetate attenuates the activation of CD4+ T cells by modulating STAT1 and −3 signaling in glia

Ahn

Jeon

Chang

et al. 2017

Sci Rep

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Interactions between immune effector cells of the central nervous system appear to directly or indirectly influence the progress/regression of multiple sclerosis (MS). Here, we report that glial STAT1 and −3 are distinctively phosphorylated following the interaction of activated lymphocytes and glia, and this effect is significantly inhibited by glatiramer acetate (GA), a disease-modifying drug for MS. GA also reduces the activations of STAT1 and −3 by MS-associated stimuli such as IFNγ or LPS in primary glia, but not neurons. Experiments in IFNγ- and IFNγ receptor-deficient mice revealed that GA-induced inhibitions of STAT signaling are independent of IFNγ and its receptor. Interestingly, GA induces the expression levels of suppressor of cytokine signaling-1 and −3, representative negative regulators of STAT signaling in glia. We further found that GA attenuates the LPS-triggered enhancement of IL-2, a highly produced cytokine in patients with active MS, in CD4+ T cells co-cultured with glia, but not in CD4+ T cells alone. Collectively, these results provide that activation of glial STATs is an essential event in the interaction between glia and T cells, which is a possible underlying mechanism of GA action in MS. These findings provide an insight for the development of targeted therapies against MS.

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“…In this study, we showed a similar increase in IL-1RN, IL-6, IL-8, IL-10, IFN-g, and TNF production induced by LPS, consistent with previous studies. [33][34][35][36] We extended those observations to show that LPS also increased the secretion of other inflammatory-related cytokines, including proinflammatory cytokines IL-1B, IL-2, IL-12p70, IL-15, and IL-17A and anti-inflammatory cytokines IL-4, IL-9; chemokines MCP-1, MIP-1a, MIP-1b, RANTES, IP-10, eotaxin, and growth factors, CSF-3, CSF-2, and VEGFA. To our knowledge, this is the first description of secretion of these cytokines, chemokines, and growth factors in human decidual cells in response to LPS in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have demonstrated that LPS induces IL-1RN, IL-6, IL-8, IL-10, IFN-g, and TNF-a output from human choriodecidual tissues or cells in vitro, using a traditional enzyme-linked immunosorbent assay (ELISA). [33][34][35][36] Obviously, studies focused on the actions of individual cytokines may not be sufficient for understanding the mechanism of PTB related to infection or inflammation. Because many cytokines that accompany inflammation have closely related or overlapping biological effects and may be involved in different aspects of immune responses, quantitation of single cytokines may be of limited value.…”

Section: Introductionmentioning

confidence: 99%

Lipopolysaccharide-Induced Profiles of Cytokine, Chemokine, and Growth Factors Produced by Human Decidual Cells Are Altered by Lactobacillus rhamnosus GR-1 Supernatant

Yang

Kim

et al. 2014

Reprod. Sci.

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Lipopolysaccharide (LPS)-induced Interferon (IFN)-gamma Production by Decidual Mononuclear Cells (DMNC) is Interleukin (IL)-2 and IL-12 Dependent

Abstract: IL-2 and IL-12 up-regulated the production of IFN-γ in DMNC through increasing their susceptibility to LPS. TNF-α production is independent of such a mechanism.

Cited by 15 publications

References 41 publications

Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms

Yohimbine Enhances Protection of Berberine against LPS-Induced Mouse Lethality through Multiple Mechanisms

Glatiramer acetate attenuates the activation of CD4+ T cells by modulating STAT1 and −3 signaling in glia

Lipopolysaccharide-Induced Profiles of Cytokine, Chemokine, and Growth Factors Produced by Human Decidual Cells Are Altered by Lactobacillus rhamnosus GR-1 Supernatant

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