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A fungal metabolite zearalenone as a CFTR inhibitor and potential therapy of secretory diarrheas.

Overstimulation of CFTR-mediated Clsecretion plays an important role in the pathogenesis of secretory diarrheas, which remain an important global health problem. This study aimed to identify inhibitors of CFTR-mediated Clsecretion from a library of fungus-derived compounds and to evaluate their pharmacological properties and anti-diarrheal utility. We identified zearalenone, 7'-dehydrozearalenone and 8'-hydroxyzearalenone isolated from the seagrass-derived fungus Fusarium sp. PSU-ES123 as inhibitors of CFTR-mediated Clsecretion in human intestinal epithelial (T84) cells. Being the most potent fungal metabolite capable of inhibiting CFTR-mediated Clsecretion, zearalenone reversibly inhibited CFTR Clchannel activity in T84 cells with an ICof ∼ 0.5 μM. Functional and biochemical analyses and molecular docking studies indicate that zearalenone binds to the β-estradiol binding sites in the ATP-binding pockets on NBD1 and NBD2 of CFTR. Mechanisms of CFTR inhibition by zearalenone do not involve activation of phosphodiesterases, protein phosphatases, multidrug-resistance protein 4 and AMP-activated protein kinases. Importantly, zearalenone significantly inhibited cholera toxin (CT)-induced Clsecretion in T84 cells and blocked CT-induced intestinal fluid secretion in mice. Collectively, our study indicates that zearalenone represents the first class of fungus-derived CFTR inhibitors. Further development of this class of compounds may provide an effective treatment of secretory diarrheas.

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EMAP-II Inhibitor Z-ASTD- EMAP-II Inhibitor Z-ASTD- EMAP II Inhibitor Z ASTD EMAP II Inhibitor Z ASTD Cell Meter™ JC 10 Mitoc Cell Meter™ JC 10 Mitoc Cell Meter™ NIR Mitocho Cell Meter™ NIR Mitocho Cell Meter™ Mitochondri MMP-13 inhibitor assay ki MMP13 inhibitor assay kit Screen Quest™ Membrane

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Neutralization of IL-17C reduces skin inflammation in mouse models of psoriasis and atopic dermatitis.

Interleukin-17C (IL-17C) is a functionally distinct member of the IL-17 family that was implicated to play a role in the pathogenesis of psoriasis. Here we confirmed that IL-17C is involved in psoriasis and explored potential roles for IL-17C in atopic dermatitis (AD). An anti-IL-17C antibody, MOR106, was generated that potently and selectively binds to human and mouse IL-17C, thereby inhibiting the binding of IL-17C to its IL-17RE receptor. The antibody inhibited cutaneous inflammation in an IL-23-induced psoriatic-like skin inflammation model. In lesional skin of patients with AD, IL-17C expression levels were increased and localized to keratinocytes and infiltrating immune cells. To determine the contribution of IL-17C to AD pathogenesis, MOR106 was tested in two distinct in vivo models. In the calcipotriol-induced AD model, ear skin inflammation, TSLP and IL-33 protein production in ears was suppressed by MOR106. Consistently, in the flaky tail strain mouse model, spontaneous development of AD-like skin inflammation was reduced by MOR106. Moreover, serum IgE levels, number of mast cells in skin and Th2 related cytokines IL-4 and CCL17 in serum were all reduced. Overall, our results indicate that IL-17C is a central mediator of skin inflammation beyond psoriasis and is relevant in particular in AD.

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Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Mouse Anti-Human Interleu Mouse Anti-Human Interleu Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Mouse Anti-Human Interleu Mouse Anti-Human Interleu Mouse Anti-Human Interleu Mouse Anti-Human Interleu

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Anti-human SIRPα antibody is a new tool for cancer immunotherapy.

Interaction of signal regulatory protein α (SIRPα) expressed on the surface of macrophages with its ligand CD47 expressed on target cells negatively regulates phagocytosis of the latter cells by the former. We recently showed that blocking Abs to mouse SIRPα enhanced both the Ab-dependent cellular phagocytosis (ADCP) activity of mouse macrophages for Burkitt's lymphoma Raji cells opsonized with an Ab to CD20 (rituximab) in vitro as well as the inhibitory effect of rituximab on the growth of tumors formed by Raji cells in nonobese diabetic/severe combined immunodeficient (NOD/SCID) mice. However, the effects of blocking Abs to human SIRPα in preclinical cancer models have remained unclear given that such Abs have failed to interact with endogenous SIRPα expressed on macrophages of immunodeficient mice. With the use of Rag2γmice harboring a transgene for human SIRPα under the control of human regulatory elements (hSIRPα-DKO mice), we here show that a blocking Ab to human SIRPα significantly enhanced the ADCP activity of macrophages derived from these mice for human cancer cells. The anti-human SIRPα Ab also markedly enhanced the inhibitory effect of rituximab on the growth of tumors formed by Raji cells in hSIRPα-DKO mice. Our results thus suggest that the combination of Abs to human SIRPα with therapeutic Abs specific for tumor antigens warrants further investigation for potential application to cancer immunotherapy. In addition, humanized mice, such as hSIRPα-DKO mice, should prove useful for validation of the antitumor effects of checkpoint inhibitors before testing in clinical trials. This article is protected by copyright. All rights reserved.

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MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI HUMAN CD19 RPE MOUSE ANTI HUMAN CD15, Pr MOUSE ANTI BOVINE ROTAVIR Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Mouse anti Human IgA anti Mouse anti Human IgE anti Mouse anti Human IgE anti Mouse anti Human IgE anti Mouse anti Human IgE anti Mouse anti Human IgG anti

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Bile Salt Hydrolase Activities: A Novel Target to Screen Anti-Lactobacilli?

is a protozoan parasite responsible for giardiasis, a disease characterized by intestinal malabsorption, diarrhea and abdominal pain in a large number of mammal species. Giardiasis is one of the most common intestinal parasitic diseases in the world and thus a high veterinary, and public health concern. It is well-established that some probiotic bacteria may confer protection against this parasiteandand we recently documented the implication of bile-salt hydrolase (BSH)-like activities from strain La1 ofas mediators of these effects. We showed that these activities were able to generate deconjugated bile salts that were toxic to the parasite. In the present study, a wide collection of lactobacilli strains from different ecological origins was screened to assay their anti-giardial effects. Our results revealed that the anti-parasitic effects of some of the strains tested were well-correlated with the expression of BSH-like activities. The two most active strains, La1 andCNCM I-4884, were then tested for their capacity to influenceinfection in a suckling mice model. Strikingly, onlyCNCM I-4884 strain was able to significantly antagonize parasite growth with a dramatic reduction of the trophozoites load in the small intestine. Moreover, this strain also significantly reduced the fecal excretion ofcysts after 5 days of treatment, which could contribute to blocking the transmission of the parasite, in contrast of La1 where no effect was observed. This study represents a step toward the development of new prophylactic strategies to combatinfection in both humans and animals.

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Rabbit Anti-Clostridium b MOUSE ANTI BOVINE ROTAVIR Rabbit Anti-alpha-Tocophe Mouse Anti-Human Prolyl H Mouse Anti-Human Prolyl H Sheep Anti-Rat Tyrosine H MOUSE ANTI BORRELIA BURGD D-Alanine Benzyl Ester p- L-Alanine Benzyl Ester p- (2S)-2-Amino-benzenebutan (1R,3S,5R)-2-Azabicyclo[3 RABBIT ANTI GSK3 BETA (pS

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A reappraisal of CTLA-4 checkpoint blockade in cancer immunotherapy.

It is assumed that anti-CTLA-4 antibodies cause tumor rejection by blocking negative signaling from B7-CTLA-4 interactions. Surprisingly, at concentrations considerably higher than plasma levels achieved by clinically effective dosing, the anti-CTLA-4 antibody Ipilimumab blocks neither B7 trans-endocytosis by CTLA-4 nor CTLA-4 binding to immobilized or cell-associated B7. Consequently, Ipilimumab does not increase B7 on dendritic cells (DCs) from either CTLA4 gene humanized (Ctla4) or human CD34stem cell-reconstituted NSG™ mice. In Ctla4mice expressing both human and mouse CTLA4 genes, anti-CTLA-4 antibodies that bind to human but not mouse CTLA-4 efficiently induce Treg depletion and Fc receptor-dependent tumor rejection. The blocking antibody L3D10 is comparable to the non-blocking Ipilimumab in causing tumor rejection. Remarkably, L3D10 progenies that lose blocking activity during humanization remain fully competent in inducing Treg depletion and tumor rejection. Anti-B7 antibodies that effectively block CD4 T cell activation and de novo CD8 T cell priming in lymphoid organs do not negatively affect the immunotherapeutic effect of Ipilimumab. Thus, clinically effective anti-CTLA-4 mAb causes tumor rejection by mechanisms that are independent of checkpoint blockade but dependent on the host Fc receptor. Our data call for a reappraisal of the CTLA-4 checkpoint blockade hypothesis and provide new insights for the next generation of safe and effective anti-CTLA-4 mAbs.

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Multiple organ cancer tis Kidney disease spectrum ( Bladder cancer tissue arr Bladder cancer tissue arr Breast cancer tissue arra Multiple breast cancer ti Breast cancer tissue arra Breast cancer and normal Breast cancer and normal Breast cancer and normal Breast cancer tissue arra Breast cancer tissue arra

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Antitumor activities of Quercetin and Green Tea in xenografts of human leukemia HL60 cells.

Quercetin is one of the most abundant flavonoids, present in fruits and vegetables and has been shown to have multiple properties capable of reducing cell growth in cancer cells. Green tea is a widely consumed beverage, known for a potential source of free radical scavenging and anti-cancer activities. Herein, we investigate the in vivo antitumor efficacy of quercetin and green tea in human leukemia. Human tumors were xenografted into NOD/SCID mice. Quercetin and green tea reduced tumor growth in HL-60 xenografts accompanied by decreased expression of anti-apoptotic proteins, BCL-2, BCL-XL and MCL-1 and increased expression of BAX, a pro-apoptotic protein. Moreover, caspase-3 was activated to a greater extent after quercetin and green tea treatment. Quercetin and green tea also mediated G1 phase cell cycle arrest in HL-60 xenografts. Treatment with quercetin and green tea induced conversion of LC3-I to LC3-II as well as activation of autophagy proteins, suggesting that quercetin and green tea initiate the autophagic progression. We have provided evidence that quercetin and green tea induces signaling at the level of apoptosis, cell cycle and autophagy which converge to antigrowth effects in HL-60 xenograft mice suggesting that these compounds may be a compelling ally in cancer treatment.

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Macrophage Colony Stimula Macrophage Colony Stimula Human Small Intestine Mic Human Large Intestine Mic Human Internal Mammary Ar GFP Expressing Human Inte Anti C Reactive Protein A Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl

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Dopamine D2 receptor up-regulates leptin and IL-6 in adipocytes.

Leptin is a pro-inflammatory cytokine secreted by the adipose tissue. Dopamine D2 receptors (D2R) have anti-inflammatory effects in the brain and kidney tissues. Mouse and human adipocytes express the (D2R); D2R protein was 10-fold greater in adipocytes from human visceral than subcutaneous tissue. However, the function of D2R in adipocytes is not well understood. The D2-like receptor agonist Quinpirole increased the protein expression of leptin and IL-6, not adiponectin and Visfatin, along with their mRNA expression (24 hr). It also increased the mRNA expression of TNF-alpha, MCP1 and NFkB-p50 (24 hr). An acute increase in the protein expression of leptin (15 min, 30min, 2 hr) and TNF-alpha (30 min) was also found in the cells treated with quinpirole. The leptin concentration in the culture media was increased by quinpirole bathing the 3T3-L1 adipocytes. These effects were prevented by the D2R antagonist L741,626. Similarly, siRNA-mediated silencing of Drd2 decreased the leptin and IL-6 and mRNA and protein expressions. The D2R-mediated increase in leptin expression was prevented by the PI3K inhibitor LY294002. The quinpirole treatment in C57Bl/6J mice increased serum leptin concentration and leptin mRNA in visceral adipocyte tissue but not in subcutaneous adippocytes confirming the stimulatory effect of D2R on leptin in vivo. Our results suggest that the stimulation of D2R increases leptin production and may have tissue specific pro-inflammatory effect in adipocytes.

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Mouse Anti-Human Interleu Androgen Receptor (Ab 650 Rabbit Anti-Leptin recept Rabbit Anti-Insulin Recep Rabbit Anti-Insulin Recep Rabbit Anti-Leptin recept Rabbit Anti-Insulin Recep Human soluble interleukin Goat Anti- Dopamine recep Goat Anti-Human Leptin Re Goat Anti-Human Nogo 66 r Interleukins Recombinant

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Babesia microti thioredoxin 3 is an effective antioxidant and involved in the response to antiprotozoal drugs.

The intra-erythrocytic apicomplexan Babesia microti is the predominant pathogen that causes human babesiosis, an infectious disease that occurs worldwide. B. microti relies on the antioxidant including thioredoxin system to maintain the redox balance during the erythrocytic stage. In the present study, the full-length B. microti thioredoxin 3 (BmTrx3) gene was cloned, expressed in vitro, and its response to antiprotozoal drugs were tested. The full-length BmTrx3 was 663 bp and contained an intact open reading frame of 567 bp. The encoded polypeptide was 188 amino acids and the predicted molecular weight of the protein was 21.7 kDa. A conserved thioredoxin-like family domain was found in BmTrx3. The expression of BmTrx3 was upregulated on both the third and eighth day post-infection in mice, whereas expression was downregulated during the beginning and later stages. Western blot analysis showed that mouse anti-BmTrx3 serum could recognize the native BmTrx3 in parasite lysates and that the mouse anti-B. microti serum could recognize the recombinant BmTrx3 protein. Immunofluorescence microscopy showed that BmTrx3 localized in the cell cytoplasm of B. microti merozoites in B. microti-infected red blood cells. The results of bovine insulin reduction assay indicated the enzyme activity of the purified recombinant BmTrx3 protein. The anti-malaria drug chloroquine significantly inhibited the expression of BmTrx3, however, another anti-malaria drug qunine, and a known anti-babesiosis drug clindamycin, induced significantly higher upregulation of BmTrx3 mRNA. The results of the present study demonstrate that BmTrx3 is a functional enzyme with antioxidant activity and may be involved in the response of B. microti to anti-parasite drugs.

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Targeting CD6 for the treatment of experimental autoimmune uveitis.

CD6 is emerging as a new target for treating many pathological conditions in which T cells are integrally involved, but even the latest data from studies of CD6 gene engineered mice were still contradictory. To address this issue, we studied experimental autoimmune uveitis (EAU), a model of autoimmune uveitis, in wild-type (WT) and CD6 knockout (KO) mice.

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Microglial activation and amyloid-β clearance induced by exogenous heat-shock proteins.

SPECIFIC AIMS We addressed the hypothesis that extracellular heat shock proteins (HSPs) induce microglial activation resulting in cytokine production and clearance of amyloid-β peptide (Aβ). The effects of exogenous HSP90, HSP70, and HSP32 on the production of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) and the phagocytosis of Aβ(1-42) were studied in isolated microglial cultures from rat and Toll-like receptor 4 (TLR4) mutant mouse brains; levels of expression and localization of HSP90 were investigated in the brains of patients with Alzheimer's disease (AD). PRINCIPAL FINDINGS 1. Exogenous HSPs induce cytokine production In rat microglial culture, addition of HSP90, HSP70, or HSP32 markedly induced production of IL-6 or TNF-α in a concentration-dependent manner whereas HSP27 did not, even at 10 μg/ml (Fig. 1 ⤻ A, B). To exclude the possibility of endotoxin contamination, samples of HSPs and lipopolysaccharide (LPS) from E. coli were heat treated at 100°C for 20 min to inactivate protein but not LPS activity before incubation with the microglia. Heat treatment completely abolished HSP90-, HSP70-, and HSP32-related induction of IL-6 and TNF-α (Fig. 1C, D ⤻ ) but, as expected, did not affect the induction of cytokine production by LPS. In contrast, 10 μg/ml of polymyxin B, which is an LPS trapper and blocks LPS-induced cellular activation, completely abolished LPS-induced production of IL-6 and TNF-α but had no effect on cytokine production induced by HSP90, HSP70, or HSP32 (Fig. 1C, D ⤻ ). Thus, microglial activation by HSPs is unlikely to be due to endotoxin contamination. [Figure: see text] 2. Exogenous HSPs enhanced phagocytosis and clearance of Aβ(1-42) At 1 day after addition of Aβ(1-42) into the culture, it was phagocytosed into rat microglia in a concentration-dependent manner. At that time, aggregated peptides of Aβ(1-42) were also detected by immunoblotting with anti-Aβ antibody. Laser confocal microscopy showed Aβ immunoreactivity in small vesicles in some microglia. The amount of Aβ(1-42) in the microglia was significantly increased after the administration of 5 μg/ml of HSP90 (56 nM), HSP70 (71 nM), or HSP32 (156 nM) but not after administration of IL-6 or TNF-α (Fig. 2 ⤻ ). The number of microglia that phagocytosed Aβ(1-42) was markedly increased: after 3 days, the amount of Aβ(1-42) detected in the microglia was significantly decreased by treatment with these HSPs vs. vehicle (Fig. 2) ⤻ . Thus, exogenous HSPs significantly facilitated the phagocytosis and clearance of Aβ(1-42) by microglia. [Figure: see text] 3. The TLR4 pathway is involved in HSP-induced microglial activation To clarify the mechanism underlying the effects of exogenous HSPs on cytokine production and Aβ clearance, the degradation of nuclear factor (NF) -κB inhibitor (IκB), phosphorylation of p38 mitogen-activated protein kinase (MAPK), and influence of TLR4-mutation were assessed. In rat microglia, the administration of 5 μg/ml of HSPs significantly induced IκB degradation and p38 MAPK phosphorylation similar to the effect of LPS. In TLR4 mutant microglia, however, production of IL-6 and TNF-α and the enhancement of Aβ phagocytosis induced by HSPs were almost completely suppressed. TLR4 mutant microglia showed a marked reduction in HSP-induced IκB degradation and p38 MAPK phosphorylation. Thus, exogenous HSPs induce NF-κB and p38 MAPK activation through TLR4. 4. HSP90 associates with Aβ plaques in AD brain After in vitro incubation of Aβ(1-42) with HSPs, Aβ was immunoprecipitated by antibodies against HSP90, HSP70, or HSP32. When rat microglia were incubated with HSPs in the presence of Aβ(1-42), IL-6 and TNF-α were produced at levels similar to when cells were treated with HSP alone. The level of expression of HSP90 in cytosolic and membranous fractions of the temporal cortex of AD brains was significantly higher than that in age-matched controls. Consistent with our in vitro studies, HSP90 immunoreactivity was colocalized with Aβ immunoreactivity. Extracellular HSP90 immunoreactivity was observed close to the microglia that expressed the human leukocyte antigen DR, a marker of reactive microglia, in senile plaques. These immunocytochemical results suggest that extracellular HSP90 accumulates close to the microglia in senile plaques. CONCLUSIONS A characteristic of AD is the accumulation of fibrillar Aβ to form amyloid plaques. Understanding the balance of production and clearance of Aβ is the key to understanding amyloid plaque homeostasis. Microglia associated with the senile plaques are likely to play a major role in this process. We showed that HSPs, such as HSP90, HSP70, and HSP32, but not HSP27, induce the production of IL-6 and TNF-α. The effect of HSPs is mediated by NF-κB and/or p38 MAPK activation through TLR4. HSP90, HSP70, and HSP32 increased the amount of Aβ in the microglia after 1 day and decreased the amount after 3 days. Addition of Aβ(1-42) alone did not induce the production of IL-6 and TNF-α, but Aβ(1-42) at lower concentrations was taken up by microglia. Although production of IL-6 and TNF-α was induced by exogenous HSPs, these cytokines did not affect the phagocytosis of Aβ by microglia. Therefore, exogenous HSPs act directly via the TLR4 pathway to induce microglial activation and facilitate the phagocytosis and clearance of Aβ (Fig. 3 ⤻ ). We demonstrated that HSP90 was also significantly increased in both the cytosolic and particulate fractions of AD brains and that extracellular HSP90 is colocalized with Aβ plaques. HSP90, HSP70, and HSP32 bound to Aβ(1-42) in vitro and, in the presence of Aβ(1-42), induced cytokine production with a potency similar to that induced by treatment with HSP alone. These observations suggest that when these HSPs are found in the extracellular milieu, they may exert chaperone and regulatory effects on various immunocompetent cells present in regions where the neurons degenerate in AD. [Figure: see text] It has been reported that IL-6 immunoreactivity is observed in senile plaques and that the TNF-α level is elevated in sera from AD patients. Since IL-6 and TNF-α are known to be proinflammatory cytokines in the immune system, microglial activation and these cytokines had been considered to exacerbate neurodegeneration. However, since recent reports have shown that IL-6 and TNF-α inhibit neuronal cell death, these cytokines may actually play a neuroprotective role in the brain (Fig. 3) ⤻ . More recently, immunization with Aβ peptides was reported to reduce the Aβ burden in transgenic mice displaying Aβ plaques. Antibodies to Aβ administered peripherally enter the brain and increase Aβ clearance, a process mediated by Fc receptors in microglia. Our findings suggest that microglial Aβ clearance induced by exogenous HSPs is mediated by activation of NF-κB and/or p38 MAPK via the TLR4 pathway. Thus, HSP-induced clearance of Aβ is mediated by a mechanism different from the clearance by antibodies to Aβ. We believe that HSP-induced microglial activation participates in compensatory neuroprotection through the production of cytokines, enhancement of phagocytosis, and clearance of Aβ. HSPs may be another option (along with anti-Aβ antibodies) to investigate in the search for a therapeutic strategy for AD.To read the full text of this article, go to http://www.fasebj.org/cgi/doi/10.1096/fj.01-0530fje ; to cite this article, use FASEB J. (February 25, 2002) 10.1096/fj.01-0530fjeThe first two authors contributed equally to this work.

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