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Immunology
NBS-LRR Protein Pik-H4 Interacts with OsBIHD1 to Balance Rice Blast Resistance and Growth by Coordinating Ethylene-Brassinosteroid Pathway
Feb 21, 2017   Frontiers In Plant Science
Liu H, Dong S, Gu F, Liu W, Yang G, Huang M, Xiao W, Liu Y, Guo T, Wang H, Chen Z, Wang J
NBS-LRR Protein Pik-H4 Interacts with OsBIHD1 to Balance Rice Blast Resistance and Growth by Coordinating Ethylene-Brassinosteroid Pathway
Feb 21, 2017
Frontiers In Plant Science
UNASSIGNED: The regulation of innate immunity and plant growth, along with the trade-off between them, affects the defense and recovery mechanisms of the plant after it is attacked by pathogens. Although it is known that hormonal crosstalk plays a major role in regulating interaction of plant growth and PAMP-triggered immunity, the relationship between plant growth and effector-triggered immunity (ETI) remains unclear. In a large-scale yeast two-hybrid screening for Pik-H4-interacting proteins, a homeodomain transcription factor OsBIHD1 was identified, which is previously known to function in biotic and abiotic stress responses. The knockout of
Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection
Feb 21, 2017   Journal Of Innate Immunity
Lin CK, Kazmierczak BI
Inflammation: A Double-Edged Sword in the Response to Pseudomonas aeruginosa Infection
Feb 21, 2017
Journal Of Innate Immunity
UNASSIGNED: The Gram-negative opportunistic pathogen Pseudomonas aeruginosa exploits failures of barrier defense and innate immunity to cause acute infections at a range of anatomic sites. We review the defense mechanisms that normally protect against P. aeruginosa pulmonary infection, as well as the bacterial products and activities that trigger their activation. Innate immune recognition of P. aeruginosa is critical for pathogen clearance; nonetheless, inflammation is also associated with pathogen persistence and poor host outcomes. We describe P. aeruginosa adaptations that improve this pathogen's fitness in the inflamed airway, and briefly discuss strategies to manipulate inflammation to benefit the host. Such adjunct therapies may become increasingly important in the treatment of acute and chronic infections caused by this multi-drug-resistant pathogen. © 2017 S. Karger AG, Basel.
Substance P represents a novel first-line defense mechanism in the nose
Feb 21, 2017   The Journal Of Allergy And Clinical Immunology
Larsson O, Tengroth L, Xu Y, Uddman R, Georén SK, Cardell LO
Substance P represents a novel first-line defense mechanism in the nose
Feb 21, 2017
The Journal Of Allergy And Clinical Immunology
BACKGROUND: Neuropeptides, such as substance P (SP), have long been seen as mediators of widespread, continuous airway inflammation, a process known as neurogenic inflammation. However, this has been difficult to demonstrate clinically, suggesting an alternative role for these signaling molecules. OBJECTIVES: To examine the role of SP in nasal infection, by assessing the release of SP in response to viral stimulation and characterizing the effects of SP on innate immunity, the latter reflected in changes in local Toll-like receptor (TLR) expression. METHODS: The distribution of SP and TLRs in the nasal mucosa and in local airway neurons was assessed with immunohistochemistry. The TLR7 agonists R-837 and R-848 were used to mimic a viral insult in upper airways, represented by primary human and mouse nasal epithelial cells (HNEC, MNEC) and isolated murine trigeminal ganglia (TGN). SP release from HNEC, MNEC and TGN was quantified with EIA. The effects of SP on TLR expression on HNEC were determined using flow cytometry and confocal microscopy. RESULTS: SP was released from the sensory neurons, MNEC and HNEC within 15 minutes of local TLR7 stimulation. Subsequently, stimulation with SP induced upregulation of TLR expression in HNEC within 30 minutes, via induction of TLR movement within HNEC. Upregulation of TLR expression was not evident when cells were treated with the neurokinin 1 receptor (NK1R) antagonist aprepitant prior to SP stimulation. CONCLUSIONS: This highlights a novel role for sensory neuropeptides as acute and local mediators of pathogen-driven inflammation, rapidly priming innate immune defenses in the airway. Copyright © 2017. Published by Elsevier Inc.
Promising Targets for Cancer Immunotherapy: TLRs, RLRs, and STING-Mediated Innate Immune Pathways
Feb 20, 2017   International Journal Of Molecular Sciences
Li K, Qu S, Chen X, Wu Q, Shi M
Promising Targets for Cancer Immunotherapy: TLRs, RLRs, and STING-Mediated Innate Immune Pathways
Feb 20, 2017
International Journal Of Molecular Sciences
UNASSIGNED: Malignant cancers employ diverse and intricate immune evasion strategies, which lead to inadequately effective responses of many clinical cancer therapies. However, emerging data suggest that activation of the tolerant innate immune system in cancer patients is able, at least partially, to counteract tumor-induced immunosuppression, which indicates triggering of the innate immune response as a novel immunotherapeutic strategy may result in improved therapeutic outcomes for cancer patients. The promising innate immune targets include Toll-like Receptors (TLRs), RIG-I-like Receptors (RLRs), and Stimulator of Interferon Genes (STING). This review discusses the antitumor properties of TLRs, RLRs, and STING-mediated innate immune pathways, as well as the promising innate immune targets for potential application in cancer immunotherapy.
Human NLRP3 inflammasome activity is regulated by and potentially targetable via BTK
Feb 20, 2017   The Journal Of Allergy And Clinical Immunology
Liu X, Pichulik T, Wolz OO, Dang TM, Stutz A,   . . . . . .   , Grimbacher B, Miller L, Brunner C, Wolz C, Weber AN
Human NLRP3 inflammasome activity is regulated by and potentially targetable via BTK
Feb 20, 2017
The Journal Of Allergy And Clinical Immunology
BACKGROUND: The Nod-like receptor, NACHT, LRR and PYD domains-containing protein 3 (NLRP3), and Bruton's tyrosine kinase (BTK) are protagonists in innate and adaptive immunity, respectively: NLRP3 senses exogenous and endogenous insults leading to inflammasome activation, which occurs spontaneously in Muckle-Wells Syndrome (MWS); BTK mutations cause the genetic immunodeficiency X-linked agammaglobulinemia (XLA). However, to date few proteins that regulate NLRP3 inflammasome activity in human primary immune cells have been identified and clinically promising pharmacological targeting strategies remain elusive. OBJECTIVE: We therefore sought to identify novel regulators of the NLRP3 inflammasome in human cells with a view to exploring interference with inflammasome activity at the level of such regulators. METHODS: Following proteome-wide phospho-proteomics, an identified novel regulator, BTK, was studied in human and murine cells using pharmacological and genetic BTK ablation. RESULTS: We here show that BTK is a critical regulator of NLRP3 inflammasome activation: Pharmacological (using the Food and Drug Administration (FDA)-approved inhibitor, ibrutinib) and genetic (in XLA patients and Btk-knockout mice) BTK ablation in primary immune cells led to reduced Interleukin (IL)-1β processing and secretion in response to Nigericin and the Staphylococcus aureus toxin, Leukocidin (Luk) AB. BTK affected Apoptosis-associated speck-like protein containing a CARD (ASC) speck formation and caspase-1 cleavage and interacted with NLRP3 and ASC. S. aureus infection control in vivo and IL-1β release from MWS patient cells were impaired by ibrutinib. Notably, IL-1β processing and release from immune cells isolated from cancer patients on ibrutinib therapy was reduced. CONCLUSION: Our data suggest that XLA may partially result from genetic inflammasome deficiency and that NLRP3 inflammasome-linked inflammation could potentially be targeted pharmacologically via BTK. Copyright © 2017. Published by Elsevier Inc.
Expression analysis of nine Toll-like receptors in yellow catfish (Pelteobagrus fulvidraco) responding to Aeromonas hydrophila challenge
Feb 22, 2017   Fish & Shellfish Immunology
Zhang XT, Zhang GR, Shi ZC, Yuan YJ, Zheng H, Lin L, Wei KJ, Ji W
Expression analysis of nine Toll-like receptors in yellow catfish (Pelteobagrus fulvidraco) responding to Aeromonas hydrophila challenge
Feb 22, 2017
Fish & Shellfish Immunology
UNASSIGNED: Toll-like receptors (TLRs) are important components of pattern recognition receptors (PRRs), which play significant roles in innate immunity to defense against pathogen invasion. Many TLRs have been found in teleosts, but there are no reports about cloning and expression of TLR genes in yellow catfish (Pelteobagrus fulvidraco). In this study, we analyzed the sequence characters and the relative mRNA expression levels of nine TLRs (TLR1, TLR2, TLR3, TLR4-1, TLR5, TLR7, TLR8-2, TLR9 and TLR22) in different tissues of yellow catfish. The results showed that all nine TLR genes are highly expressed in head kidney, trunk kidney, spleen and liver, all of which are related to host immunity. Subsequently we used Aeromonas hydrophila as a stimulating agent to detect the expression profiles of these nine TLRs in the liver, spleen, trunk kidney and head kidney of yellow catfish at different time points after injection with killed Aeromonas hydrophila. All nine TLRs responded to A. hydrophila challenge with tissue-specific patterns in different immune tissues. The kinetics of up- or down-regulation of these nine TLRs exhibited a similar trend, rising to an elevated level at first and then falling to the basal level, but the peak value differed at different time points in different tissues. The expression levels of the TLR3, TLR4-1, TLR9 and TLR22 genes were significantly up-regulated after bacterial challenge in the liver, spleen, head kidney and trunk kidney. The relatively high expression of TLR genes in the immune tissues in response to the A. hydrophila challenge indicated that TLRs may play important roles in the innate immune response against gram-negative bacteria in yellow catfish. Copyright © 2017. Published by Elsevier Ltd.
Resolution of TLR2-induced inflammation through manipulation of metabolic pathways in Rheumatoid Arthritis
Feb 22, 2017   Scientific Reports
McGarry T, Biniecka M, Gao W, Cluxton D, Canavan M, Wade S, Wade S, Gallagher L, Orr C, Veale DJ, Fearon U
Resolution of TLR2-induced inflammation through manipulation of metabolic pathways in Rheumatoid Arthritis
Feb 22, 2017
Scientific Reports
UNASSIGNED: During inflammation, immune cells activated by toll-like receptors (TLRs) have the ability to undergo a bioenergetic switch towards glycolysis in a manner similar to that observed in tumour cells. While TLRs have been implicated in the pathogenesis of rheumatoid arthritis (RA), their role in regulating cellular metabolism in synovial cells, however, is still unknown. In this study, we investigated the effect of TLR2-activation on mitochondrial function and bioenergetics in primary RA-synovial fibroblast cells (RASFC), and further determined the role of glycolytic blockade on TLR2-induced inflammation in RASFC using glycolytic inhibitor 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one (3PO). We observed an increase in mitochondrial mutations, ROS and lipid peroxidation, paralleled by a decrease in the mitochondrial membrane potential in TLR2-stimulated RASFC. This was mirrored by differential regulation of key mitochondrial genes, coupled with alteration in mitochondrial morphology. TLR2-activation also regulated changes in the bioenergetic profile of RASFC, inducing PKM2 nuclear translocation, decreased mitochondrial respiration and ATP synthesis and increased glycolysis:respiration ratio, suggesting a metabolic switch. Finally, using 3PO, we demonstrated that glycolytic blockade reversed TLR2-induced pro-inflammatory mechanisms including invasion, migration, cytokine/chemokine secretion and signalling pathways. These findings support the concept of complex interplay between innate immunity, oxidative damage and oxygen metabolism in RA pathogenesis.
Inhibition of Kupffer Cell Autophagy Abrogates Nanoparticle-Induced Liver Injury
Feb 24, 2017   Advanced Healthcare Materials
Zhu S, Zhang J, Zhang L, Ma W, Man N,   . . . . . .   , Lu X, Yang Z, Liu X, Bai L, Wen L
Inhibition of Kupffer Cell Autophagy Abrogates Nanoparticle-Induced Liver Injury
Feb 24, 2017
Advanced Healthcare Materials
The possible adverse effects of engineered nanomaterials on human health raise increasing concern as our research on nanosafety intensifies. Upon entry into a human body, whether intended for a theranostic purpose or through unintended exposure, nanomaterials tend to accumulate in the liver, leading to hepatic damage. A variety of nanoparticles, including rare earth upconversion nanoparticles (UCNs), have been reported to elicit hepatotoxicity, in most cases through inducing immune response or activating reactive oxygen species. Many of these nanoparticles also induce autophagy, and autophagy inhibition has been shown to decrease UCN-induced liver damage. Herein, using UCNs as a model engineered nanomaterial, this study uncovers a critical role for Kupffer cells in nanomaterial-induced liver toxicity, as depletion of Kupffer cells significantly exacerbates UCN-induced liver injury. Furthermore, UCN-induced prodeath autophagy in Kupffer cells, and inhibition of autophagy with 3-MA, a well-established chemical inhibitor of autophagy, enhances Kupffer cell survival and further abrogates UCN-induced liver toxicity. The results reveal the critical importance of Kupffer cell autophagy for nanoparticle-induced liver damage, and inhibition of autophagy may constitute a novel strategy for abrogating nanomaterial-elicited liver toxicity.© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
CARD and TM of MAVS of black carp play the key role in its self-association and antiviral ability
Feb 24, 2017   Fish & Shellfish Immunology
Xiao J, Yan C, Zhou W, Li J, Wu H, Chen T, Feng H
CARD and TM of MAVS of black carp play the key role in its self-association and antiviral ability
Feb 24, 2017
Fish & Shellfish Immunology
Mitochondrial antiviral signaling protein (MAVS) is an adaptor protein of the innate immune system of higher vertebrate. In this paper, the transcription profile of black carp MAVS (bcMAVS) in host cells in response to spring viremia of carp virus (SVCV) and grass carp reovirus (GCRV) infection was identified. EPC cells expressing bcMAVS possessed obviously enhanced antiviral activity against both SVCV and GCRV. Immunofluorescence (IF) staining data demonstrated that bcMAVS molecules were redistributed and formed aggregates on the mitochondria of EPC cells after virus infection. Co-immunoprecipitation (co-IP) assay in HEK293T cells demonstrated that bcMAVS proteins bound to each other, which suggested that this fish protein owned self-association in vivo. IF assay identified that the transmembrane (TM) domain of bcMAVS was crucial for its mitochondrial localization. Co-IP assays among bcMAVS mutants demonstrated that both N-terminal caspase recruitment domain (CARD) and TM domain were indispensible for dimerization of bcMAVS. It was interesting that Truncated-bcMAVS possessed much enhanced interferon-inducing activity and antiviral ability than wild type bcMAVS, which only contains CARD and TM. All the data generated in this study support the idea that oligomerization of bcMAVS on mitochondrion is crucial for the antiviral ability of bcMAVS, which is depend on both CARD and TM domain of this fish MAVS orthologue.Copyright © 2017. Published by Elsevier Ltd.
Proofreading of Peptide-MHC Complexes through Dynamic Multivalent Interactions
Feb 23, 2017   Frontiers In Immunology
Thomas C, Tampé R
Proofreading of Peptide-MHC Complexes through Dynamic Multivalent Interactions
Feb 23, 2017
Frontiers In Immunology
The adaptive immune system is able to detect and destroy cells that are malignantly transformed or infected by intracellular pathogens. Specific immune responses against these cells are elicited by antigenic peptides that are presented on major histocompatibility complex class I (MHC I) molecules and recognized by cytotoxic T lymphocytes at the cell surface. Since these MHC I-presented peptides are generated in the cytosol by proteasomal protein degradation, they can be metaphorically described as a window providing immune cells with insights into the state of the cellular proteome. A crucial element of MHC I antigen presentation is the peptide-loading complex (PLC), a multisubunit machinery, which contains as key constituents the transporter associated with antigen processing (TAP) and the MHC I-specific chaperone tapasin (Tsn). While TAP recognizes and shuttles the cytosolic antigenic peptides into the endoplasmic reticulum (ER), Tsn samples peptides in the ER for their ability to form stable complexes with MHC I, a process called peptide proofreading or peptide editing. Through its selection of peptides that improve MHC I stability, Tsn contributes to the hierarchy of immunodominant peptide epitopes. Despite the fact that it concerns a key event in adaptive immunity, insights into the catalytic mechanism of peptide proofreading carried out by Tsn have only lately been gained
Characterization and functional analysis of serpin-1 like gene from oak silkworm Antheraea pernyi
Feb 23, 2017   Bulletin Of Entomological Research
Yu HM, Zhu BJ, Sun Y, Wei GQ, Wang L, Qian C, Nadeem Abbas M, Liu CL
Characterization and functional analysis of serpin-1 like gene from oak silkworm Antheraea pernyi
Feb 23, 2017
Bulletin Of Entomological Research
Serpins are a broadly distributed family of proteases found in various organisms that play an important role in regulating the immune response. Here, we identified a serpin-1 gene from Antheraea pernyi that encodes a 279 amino acid protein with a molecular weight of 30.8 kDa. We expressed the recombinant Ap-serpin-1 protein in Escherichia coli and used the purified protein to prepare rabbit anti-Ap-serpin-1 polyclonal antibodies. We calculated the enzyme-linked immunosorbent assay titer of the antibody as 1:128000. Quantitative real-time polymerase chain reaction analysis revealed that Ap-serpin-1 was expressed in all examined tissues, including hemolymph, malpighian tubules, midgut, silk gland, integument and the fat body; the highest Ap-serpin-1 expression levels was detected in the fat body. We next investigated the expression patterns of Ap-serpin-1 in both fat body and hemolymph samples, following treatment with E. coli, Beauveria bassiana, Micrococcus luteus and nuclear polyhedrosis virus (NPV). We reported that NPV and M. luteus significantly enhanced Ap-serpin-1 expression in the fat body. While, in the hemolymph samples, treatment with B. bassiana and M. luteus was shown to upregulate Ap-serpin-1 expression at 24 h induction. Altogether, our results suggest that Ap-serpin-1 is involved in the innate immunity of A. pernyi.
Differential Responses of Human Fetal Brain Neural Stem Cells to Zika Virus Infection
Feb 20, 2017   Stem Cell Reports
McGrath EL, Rossi SL, Gao J, Widen SG, Grant AC,   . . . . . .   , Yu Y, Fernández-Salas I, Weaver SC, Vasilakis N, Wu P
Differential Responses of Human Fetal Brain Neural Stem Cells to Zika Virus Infection
Feb 20, 2017
Stem Cell Reports
UNASSIGNED: Zika virus (ZIKV) infection causes microcephaly in a subset of infants born to infected pregnant mothers. It is unknown whether human individual differences contribute to differential susceptibility of ZIKV-related neuropathology. Here, we use an Asian-lineage ZIKV strain, isolated from the 2015 Mexican outbreak (Mex1-7), to infect primary human neural stem cells (hNSCs) originally derived from three individual fetal brains. All three strains of hNSCs exhibited similar rates of Mex1-7 infection and reduced proliferation. However, Mex1-7 decreased neuronal differentiation in only two of the three stem cell strains. Correspondingly, ZIKA-mediated transcriptome alterations were similar in these two strains but significantly different from that of the third strain with no ZIKV-induced neuronal reduction. This study thus confirms that an Asian-lineage ZIKV strain infects primary hNSCs and demonstrates a cell-strain-dependent response of hNSCs to ZIKV infection. Copyright © 2017 The Authors. Published by Elsevier Inc. All rights reserved.
A NLRC3-like gene from blunt snout bream (Megalobrama amblycephala): Molecular characterization, expression and association with resistance to Aeromonas hydrophila infection
Feb 20, 2017   Fish & Shellfish Immunology
Zhou F, Zhan Q, Ding Z, Su L, Fan J, Cui L, Chen N, Wang W, Liu H
A NLRC3-like gene from blunt snout bream (Megalobrama amblycephala): Molecular characterization, expression and association with resistance to Aeromonas hydrophila infection
Feb 20, 2017
Fish & Shellfish Immunology
UNASSIGNED: NLRC (the nucleotide-oligomerization domain (NOD)-like receptor subfamily C) consists of teleost-specific NLRs (NOD-like receptors) and plays pivotal roles in microbial recognition and regulation of innate immune response. In this study, we cloned and characterized a NLRC3-like gene (MamNLRC3-like) from blunt snout bream (Megalobrama amblycephala) by using the quantitative real-time PCR method, and analyzed the correlation between its polymorphisms and resistance to Aeromonas hydrophila infection. The full length cDNA of MamNLRC3-like was 2863 bp, with a 5'-UTR of 169 bp, ORF of 2301 bp and 3'-UTR of 393 bp, encoding 766 amino acid residues. MamNLRC3-like consisted of a conserved NACHT domain, a fish-specific NACHT associated domain (FISNA) and a PYRIN effective domain. During early developmental stages, MamNLRC3-like was most highly expressed at 39.4 hpf (hours post fertilization, hatching stage) and constitutively detected in various healthy tissues. The expression of MamNLRC3-like was strongly induced by A. hydrophila infection and peaked in the head kidney, liver, intestine, and trunk kidney at 12 h post infection. Six SNPs (single nucleotide polymorphisms) from MamNLRC3-like, with 2 in introns and 4 in exons, were identified by direct sequencing, in which 6515C/T was a novel non-synonymous mutation. HRM (high resolution melting) genotyping of the 6 loci showed that locus 6515C/T SNP was associated with the resistance/susceptibility of blunt snout bream to A. hydrophila infection (P 
Tim-3 inhibits macrophage control of Listeria monocytogenes by inhibiting Nrf2
Feb 16, 2017   Scientific Reports
Wang Z, Sun D, Chen G, Li G, Dou S, Wang R, Xiao H, Hou C, Li Y, Feng J, Shen B, Han G
Tim-3 inhibits macrophage control of Listeria monocytogenes by inhibiting Nrf2
Feb 16, 2017
Scientific Reports
T cell immunoglobulin mucin-3 (Tim-3) is an immune checkpoint inhibitor and its dysregulation has been related to T cell tolerance and many immune disorders, such as tumors and infection tolerance. However, the physiopathology roles of Tim-3 in innate immunity remain elusive. Here, we demonstrate that Tim-3 inhibits macrophage phagocytosis of L. monocytogenes by inhibiting the nuclear erythroid 2-related factor 2 (Nrf2) signaling pathway and increases bacterial burden. Tim-3 signaling promotes Nrf2 degradation by increasing its ubiquitination and, as a result, decreasing its nuclear translocation. CD36 and heme oxygenase-1 (HO-1), two downstream molecules in the Tim-3-Nrf2 signaling axis, are involved in the Tim-3- mediated immune evasion of L. monocytogenes both in vitro and in vivo. We here identified new mechanisms by which Tim-3 induces infection tolerance. By modulating the Tim-3 pathway, we demonstrate the feasibility of manipulating macrophage function as a potent tool for treating infectious diseases, such as Listeria infection.
Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation
Feb 17, 2017   Scientific Reports
Jiang MX, Hong X, Liao BB, Shi SZ, Lai XF, Zheng HY, Xie L, Wang Y, Wang XL, Xin HB, Fu M, Deng KY
Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation
Feb 17, 2017
Scientific Reports
UNASSIGNED: Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. However, the molecular mechanisms limiting macrophage activation are not completely understood. Members of the tripartite motif (TRIM) family have recently emerged as important players in innate immunity and antivirus. Here, we systematically analyzed mRNA expressions of representative TRIM molecules in human THP1-derived macrophages activated by different toll-like receptor (TLR) ligands. Twenty-nine TRIM members were highly induced (>3 fold) by one or more TLR ligands, among which 19 of them belong to TRIM C-IV subgroup. Besides TRIM21, TRIM22 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identified a novel group of TRIM genes (TRIM14, 15, 31, 34, 43, 48, 49, 51 and 61) that were significantly up-regulated by TLR3 and TLR4 ligands. In contrast, the expression of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophages. The alternations of the TRIM proteins were confirmed by Western blot. Finally, overexpression of TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediated knockdown of TRIM59 enhanced LPS-induced macrophage activation. Taken together, the study provided an insight into the TLR ligands-induced expressions of TRIM family in macrophages.
Autocrine prolactin stimulates endometrial carcinoma growth and metastasis and reduces sensitivity to chemotherapy
Feb 16, 2017   Endocrinology
Ding K, Yuan Y, Chong QY, Yang Y, Li R, Li X, Kong X, Qian P, Xiong Z, Pandey V, Ma L, Wu Z, Lobie PE, Zhu T
Leukocyte TLR5 deficiency inhibits atherosclerosis by reduced macrophage recruitment and defective T-cell responsiveness
Feb 16, 2017   Scientific Reports
Ellenbroek GH, van Puijvelde GH, Anas AA, Bot M, Asbach M,   . . . . . .   , Pasterkamp G, Hoefer IE, van der Poll T, Kuiper J, de Jager SC
Leukocyte TLR5 deficiency inhibits atherosclerosis by reduced macrophage recruitment and defective T-cell responsiveness
Feb 16, 2017
Scientific Reports
Toll-like receptors (TLR) provide a critical link between innate and adaptive immunity, both important players in atherosclerosis. Since evidence for the role of TLR5 is lacking, we aimed to establish this in the immune axis of atherosclerosis. We assessed the effect of the TLR5-specific ligand Flagellin on macrophage maturation and T-cell polarisation. Next, we generated TLR5
Decreased sugar concentration in vegetable and fruit juices by growth of functional lactic acid bacteria
Feb 16, 2017   Drug Discoveries & Therapeutics
Ishii M, Matsumoto Y, Nishida S, Sekimizu K
Decreased sugar concentration in vegetable and fruit juices by growth of functional lactic acid bacteria
Feb 16, 2017
Drug Discoveries & Therapeutics
UNASSIGNED: Leuconostoc carnosum #7-2, L. gelidum #4-2, and L. mesenteroides 8/11-3, which were isolated from fermented plant foods, are lactic acid bacteria. We previously reported that these bacteria are functional lactic acid bacteria whose innate immunity-stimulating activities are high based on a silkworm muscle contraction assay. The concentrations of these three lactic acid bacteria increased to more than 1 × 10
Identification and Characterization of Lipopolysaccharide Induced TNFα Factor from Blunt Snout Bream, Megalobrama amblycephala
Feb 17, 2017   International Journal Of Molecular Sciences
Lv Y, Xiang X, Jiang Y, Tang L, Zhou Y, Zhong H, Xiao J, Yan J
Identification and Characterization of Lipopolysaccharide Induced TNFα Factor from Blunt Snout Bream, Megalobrama amblycephala
Feb 17, 2017
International Journal Of Molecular Sciences
UNASSIGNED: Lipopolysaccharide induced TNFα factor (LITAF) is an important transcription factor responsible for regulation of tumor necrosis factor α. In this study, a novel
Correction: Type I Interferon Receptor Deficiency in Dendritic Cells Facilitates Systemic Murine Norovirus Persistence Despite Enhanced Adaptive Immunity
Feb 17, 2017   PLoS Pathogens
Nice TJ, Osborne LC, Tomov VT, Artis D, Wherry EJ, Virgin HW
Mining the Human Gut Microbiota for Immunomodulatory Organisms
Feb 20, 2017   Cell
Geva-Zatorsky N, Sefik E, Kua L, Pasman L, Tan TG, Ortiz-Lopez A, Yanortsang TB, Yang L, Jupp R, Mathis D, Benoist C, Kasper DL
Mining the Human Gut Microbiota for Immunomodulatory Organisms
Feb 20, 2017
Cell
UNASSIGNED: Within the human gut reside diverse microbes coexisting with the host in a mutually advantageous relationship. Evidence has revealed the pivotal role of the gut microbiota in shaping the immune system. To date, only a few of these microbes have been shown to modulate specific immune parameters. Herein, we broadly identify the immunomodulatory effects of phylogenetically diverse human gut microbes. We monocolonized mice with each of 53 individual bacterial species and systematically analyzed host immunologic adaptation to colonization. Most microbes exerted several specialized, complementary, and redundant transcriptional and immunomodulatory effects. Surprisingly, these were independent of microbial phylogeny. Microbial diversity in the gut ensures robustness of the microbiota's ability to generate a consistent immunomodulatory impact, serving as a highly important epigenetic system. This study provides a foundation for investigation of gut microbiota-host mutualism, highlighting key players that could identify important therapeutics. Copyright © 2017 Elsevier Inc. All rights reserved.
HcToll3 was involved in anti-Vibrio defense in freshwater pearl mussel, Hyriopsis cumingii
Feb 19, 2017   Fish & Shellfish Immunology
Zhang HW, Huang Y, Man X, Wang Y, Hui KM, Yin SW, Zhang XW
HcToll3 was involved in anti-Vibrio defense in freshwater pearl mussel, Hyriopsis cumingii
Feb 19, 2017
Fish & Shellfish Immunology
UNASSIGNED: Toll-like receptors (TLRs) play an important role in the activation of innate immune response but their functions in bivalves remain largely unknown. In this study, we identified a TLR from the freshwater pearl mussel Hyriopsis cumingii (HcToll3) and investigated its functions in immunity. The full-length cDNA of HcToll3 is 3852 bp and includes an open reading frame (ORF) of 3228 bp that encodes a polypeptide of 1075 amino acids. The predicted HcToll3 protein shares similar structural characteristics with other known Toll family proteins. Quantitative real-time PCR analysis revealed that HcToll3 mRNA is broadly expressed in all of the examined tissues; its transcript level was significantly up-regulated by challenge with gram-negative bacteria Vibrio parahaemolyticus or lipopolysaccharide, but not gram-positive Staphylococcus aureus or peptidoglycan. RNA interference by siRNA results showed that HcToll3 regulated expression of whey acidic protein (HcWAP) and lysozymes (HcLyso1 and HcLyso2) in vivo and knockdown of HcToll3 suppressed the elimination of V. parahaemolyticus. These findings suggest that HcToll3 might be involved in anti-Vibrio defense in H. cumingii. Copyright © 2017. Published by Elsevier Ltd.
Three STATs are involved in the regulation of the expression of antimicrobial peptides in the triangle sail mussel, Hyriopsis cumingii
Feb 19, 2017   Fish & Shellfish Immunology
Dai YJ, Hui KM, Zhang YH, Liu Y, Wang YQ, Zhao LJ, Lin L, Chai LQ, Wei S, Lan JF
Three STATs are involved in the regulation of the expression of antimicrobial peptides in the triangle sail mussel, Hyriopsis cumingii
Feb 19, 2017
Fish & Shellfish Immunology
UNASSIGNED: Janus kinase (Jak) and signal transducers and activators of transcription (STAT) signaling pathway is associated in antiviral and antibacterial immune response. Previous studies primarily investigated the function of STATs in mammals. For most invertebrates, only one STAT was found in each species, such as STAT92E was found in Drosophila melanogaster. The studies, which focus on the functional difference between various STATs in the same species of invertebrate, are limited. In the present study, three STATs (HcSTAT1, HcSTAT2 and HcSTAT3) were identified in triangle shell pearl mussel, Hyriopsis cumingii. Phylogenetic analysis showed that HcSTAT1 and HcSTAT3 were clustered with Homo sapiens STAT5, and HcSTAT2 was clustered with Pinctada fucata STAT and Crassostea gigas STAT6. All three STATs could be detected in all tested tissues (hemocytes, hepatopancreas, gill, mantle and foot), and were induced expression when challenged with Staphylococcus aureus or Aeromonas hydrophilia in hemocytes and hepatopancreas. HcSTAT1 regulated the expression of HcDef, HcWAP, HcThe and HcTNF. The expression of HcWAP and HcTNF was down-regulated in HcSTAT2-RNAi mussel. And HcSTAT3 affected the expression of HcTNF. The study is the first report of different functions in antibacterial immune responses between STATs in mollusks. Copyright © 2017. Published by Elsevier Ltd.
Mitochondrial damage elicits a TCDD-inducible poly(ADP-ribose) polymerase-mediated antiviral response
Feb 18, 2017   Proceedings Of The National Academy Of Sciences Of The United States Of America
Kozaki T, Komano J, Kanbayashi D, Takahama M, Misawa T, Satoh T, Takeuchi O, Kawai T, Shimizu S, Matsuura Y, Akira S, Saitoh T
Mitochondrial damage elicits a TCDD-inducible poly(ADP-ribose) polymerase-mediated antiviral response
Feb 18, 2017
Proceedings Of The National Academy Of Sciences Of The United States Of America
UNASSIGNED: The innate immune system senses RNA viruses by pattern recognition receptors (PRRs) and protects the host from virus infection. PRRs mediate the production of immune modulatory factors and direct the elimination of RNA viruses. Here, we show a unique PRR that mediates antiviral response. Tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP ribose) polymerase (TIPARP), a Cysteine3 Histidine (CCCH)-type zinc finger-containing protein, binds to Sindbis virus (SINV) RNA via its zinc finger domain and recruits an exosome to induce viral RNA degradation. TIPARP typically localizes in the nucleus, but it accumulates in the cytoplasm after SINV infection, allowing targeting of cytoplasmic SINV RNA. Redistribution of TIPARP is induced by reactive oxygen species (ROS)-dependent oxidization of the nuclear pore that affects cytoplasmic-nuclear transport. BCL2-associated X protein (BAX) and BCL2 antagonist/killer 1 (BAK1), B-cell leukemia/lymphoma 2 (BCL2) family members, mediate mitochondrial damage to generate ROS after SINV infection. Thus, TIPARP is a viral RNA-sensing PRR that mediates antiviral responses triggered by BAX- and BAK1-dependent mitochondrial damage.
Lactic acid bacteria of the Leuconostoc genus with high innate immunity-stimulating activity
Feb 16, 2017   Drug Discoveries & Therapeutics
Ishii M, Nishida S, Kataoka K, Nishiyama Y, Abe S, Sekimizu K
Lactic acid bacteria of the Leuconostoc genus with high innate immunity-stimulating activity
Feb 16, 2017
Drug Discoveries & Therapeutics
UNASSIGNED: We screened lactic acid bacteria that exhibited high innate immunity-stimulating activity by monitoring muscle contraction activity in silkworms. Heat-treated fractions of lactic acid bacteria, Leuconostoc carnosum #7-2, Leuconostoc gelidum #4-2, and Leuconostoc mesenteroides 8/11-3, had high (250-460 units/mg) innate immunity-stimulating activity. These lactic acid bacteria proliferated in milk to concentrations of 1 × 10

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