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https://www.readbyqxmd.com/read/29772244/gender-difference-in-the-effect-of-progesterone-on-neonatal-hypoxic-ischemic-brain-injury-in-mouse
#1
Shuyu Dong, Qian Zhang, Delian Kong, Chao Zhou, Jie Zhou, Jingjing Han, Yan Zhou, Guoliang Jin, Xiaodong Hua, Jun Wang, Fang Hua
This study was to investigate the effects of progesterone (PROG) on neonatal hypoxic/ischemic (NHI) brain injury, the differences in effects between genders, and the underlying mechanisms. NHI brain injury was established in both male and female neonatal mice induced by occlusion of the left common carotid artery followed by hypoxia. The mice were treated with PROG or vehicle. Fluoro-Jade B staining (F-JB), long term behavior testing, and brain magnetic resonance image (MRI) were applied to evaluate neuronal death, neurological function, and brain damage...
May 14, 2018: Experimental Neurology
https://www.readbyqxmd.com/read/29760187/lipopolysaccharide-lps-binding-protein-stimulates-cd14-dependent-toll-like-receptor-4-internalization-and-lps-induced-tbk1-ikk%C3%AF%C2%B5-irf3-axis-activation
#2
Hiroki Tsukamoto, Shino Takeuchi, Kanae Kubota, Yohei Kobayashi, Sao Kozakai, Ippo Ukai, Ayumi Shichiku, Misaki Okubo, Muneo Numasaki, Yoshitomi Kanemitsu, Yotaro Matsumoto, Tomonori Nochi, Kouichi Watanabe, Hisashi Aso, Yoshihisa Tomioka
Toll-like receptor 4 (TLR4) is an indispensable immune receptor for lipopolysaccharide (LPS), a major component of the Gram-negative bacterial cell wall. Following LPS stimulation, TLR4 transmits the signal from the cell surface and becomes internalized in an endosome. However, the spatial regulation of TLR4 signaling is not fully understood. Here, we investigated the mechanisms of LPS-induced TLR4 internalization and clarified the roles of the extracellular LPS-binding molecules, LPS-binding protein (LBP), and glycerophosphatidylinositol-anchored protein (CD14)...
May 14, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29755465/irf3-negatively-regulates-toll-like-receptor-mediated-nf-%C3%AE%C2%BAb-signaling-by-targeting-trif-for-degradation-in-teleost-fish
#3
Xueyan Zhao, Ruixuan Huo, Xiaolong Yan, Tianjun Xu
NF-κB signaling is tightly regulated and essential to innate and adaptive immune responses, its regulatory mechanism remains unclear in various organisms, especially teleosts. In this study, we reported that IRF3 can negatively regulate TRIF-mediated NF-κB signaling pathway. Overexpression of IRF3 can inhibit TRIF-mediated NF-κB signaling pathway. However, knockdown of IRF3 had an opposite effect. IRF3 can promote the degradation of TRIF protein in mammal and fish cells, but this effect could be inhibited by MG132 treatment...
2018: Frontiers in Immunology
https://www.readbyqxmd.com/read/29741098/monophosphoryl-lipid-a-prevents-impairment-of-medullary-thick-ascending-limb-hco-3-absorption-and-improves-plasma-hco-3-concentration-in-septic-mice
#4
Bruns A Watts, Thampi George, Edward R Sherwood, David W Good
Metabolic acidosis is the most common acid-base disorder in septic patients and is associated with increased mortality. Previously we demonstrated that sepsis induced by cecal ligation and puncture (CLP) impairs HCO3 - absorption in the MTAL by: 1) decreasing the intrinsic HCO3 - absorptive capacity, and 2) enhancing inhibition of HCO3 - absorption by LPS through upregulation of TLR4 signaling. Both effects depend on ERK activation. Monophosphoryl lipid A (MPLA) is a detoxified TLR4 agonist that enhances innate antimicrobial immunity and improves survival following sepsis...
May 9, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/29725271/the-protective-mechanism-of-cay10683-on-intestinal-mucosal-barrier-in-acute-liver-failure-through-lps-tlr4-myd88-pathway
#5
Yao Wang, Hui Chen, Qian Chen, Fang-Zhou Jiao, Wen-Bin Zhang, Zuo-Jiong Gong
The purpose of this study was to investigate the protective mechanism of HDAC2 inhibitor CAY10683 on intestinal mucosal barrier in acute liver failure (ALF). In order to establish ALF-induced intestinal epithelial barrier disruption models, D-galactosamine/LPS and LPS were, respectively, used with rats and NCM460 cell and then administrated with CAY10683. Transepithelial electrical resistance (TEER) was measured to detect the permeability of cells. Real-time PCR and Western blotting were employed to detect the key mRNA and protein levels...
2018: Mediators of Inflammation
https://www.readbyqxmd.com/read/29722563/damage-associated-molecular-patterns-damps-in-resuscitated-hemorrhagic-shock-are-mitigated-by-peritoneal-fluid-administration
#6
Paul J Matheson, Mark A Eid, Matthew A Wilson, Victoria S Graham, Samuel A Matheson, Jessica Lee Weaver, Cynthia D Downard, Jason W Smith
INTRODUCTION: Conventional resuscitation (CR) of hemorrhagic shock (HS), a significant cause of trauma mortality, is I.V. blood and fluids. CR restores central hemodynamics, but vital organ flow can drop causing hypoperfusion, hypoxia, Damage-Associated Molecular Patterns (DAMPs), and remote organ dysfunction (i.e., lung). CR plus Direct Peritoneal Resuscitation (DPR) prevents intestinal and hepatic hypoperfusion. We hypothesized that DPR prevents lung injury in HS/CR by altering DAMPs...
May 3, 2018: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29720937/the-nlrp3-caspase-1-inflammasome-negatively-regulates-autophagy-via-tlr4-trif-in-prion-peptide-infected-microglia
#7
Mengyu Lai, Hao Yao, Syed Zahid Ali Shah, Wei Wu, Di Wang, Ying Zhao, Lu Wang, Xiangmei Zhou, Deming Zhao, Lifeng Yang
Prion diseases are neurodegenerative disorders characterized by the accumulation of misfolded prion protein, spongiform changes in the brain, and brain inflammation as a result of the wide-spread activation of microglia. Autophagy is a highly conserved catabolic process for the clearance of cytoplasmic components, including protein aggregates and damaged organelles; this process also eliminates pathological PrPSc as it accumulates during prion infection. The NALP3 inflammasome is a multiprotein complex that is a component of the innate immune system and is responsible for the release of pro-inflammatory cytokines...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29720226/increased-a20-e3-ubiquitin-ligase-interactions-in-bid-deficient-glia-attenuate-tlr3-and-tlr4-induced-inflammation
#8
Sinéad Kinsella, Michael Fichtner, Orla Watters, Hans-Georg König, Jochen H M Prehn
BACKGROUND: Chronic pro-inflammatory signaling propagates damage to neural tissue and affects the rate of disease progression. Increased activation of Toll-like receptors (TLRs), master regulators of the innate immune response, is implicated in the etiology of several neuropathologies including amyotrophic lateral sclerosis, Alzheimer's disease, and Parkinson's disease. Previously, we identified that the Bcl-2 family protein BH3-interacting domain death agonist (Bid) potentiates the TLR4-NF-κB pro-inflammatory response in glia, and specifically characterized an interaction between Bid and TNF receptor associated factor 6 (TRAF6) in microglia in response to TLR4 activation...
May 2, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29717937/deletion-or-pharmacological-blockade-of-toll-like-receptor-4-tlr4-confers-protection-against-cyclophosphamide-induced-mouse-cystitis
#9
Mariana G de Oliveira, Fabiola Zakia Mónica, Fabiano B Calmasini, Eduardo C Alexandre, Edith B G Tavares, Antonio G Soares, Soraia K P Costa, Edson Antunes
Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is a chronic inflammatory disease without consistently effective treatment. We investigate the role of toll-like receptor (TLR4) on voiding dysfunction and inflammation in the cyclophosphamide (CYP)-induced mouse cystitis. Males C57BL/6 (wild-type, WT) and/or TLR4 knockout (TLR4-/-) were treated with an injection of CYP (300 mg/kg, 24 h) or saline (10 ml/kg). The pharmacological blockade of the TLR4 by resatorvid (10 mg/kg) was also performed 1 h prior CYP-injection in WT mice...
May 2, 2018: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/29686054/the-tlr4-agonist-monophosphoryl-lipid-a-drives-broad-resistance-to-infection-via-dynamic-reprogramming-of-macrophage-metabolism
#10
Benjamin A Fensterheim, Jamey D Young, Liming Luan, Ruby R Kleinbard, Cody L Stothers, Naeem K Patil, Allison G McAtee-Pereira, Yin Guo, Irina Trenary, Antonio Hernandez, Jessica B Fults, David L Williams, Edward R Sherwood, Julia K Bohannon
Monophosphoryl lipid A (MPLA) is a clinically used TLR4 agonist that has been found to drive nonspecific resistance to infection for up to 2 wk. However, the molecular mechanisms conferring protection are not well understood. In this study, we found that MPLA prompts resistance to infection, in part, by inducing a sustained and dynamic metabolic program in macrophages that supports improved pathogen clearance. Mice treated with MPLA had enhanced resistance to infection with Staphylococcus aureus and Candida albicans that was associated with augmented microbial clearance and organ protection...
April 23, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29666475/lincrna-cox2-regulates-nlrp3-inflammasome-and-autophagy-mediated-neuroinflammation
#11
Zhenyi Xue, Zimu Zhang, Hongkun Liu, Wen Li, Xiangdong Guo, Zhihui Zhang, Ying Liu, Long Jia, Yan Li, Yinghui Ren, Hongwei Yang, Lijuan Zhang, Qi Zhang, Yurong Da, Junwei Hao, Zhi Yao, Rongxin Zhang
Inflammasome activation plays key roles in host defense, but also contributes to the pathogenesis of auto-inflammatory, and neurodegenerative diseases. As autophagy is connected with both the innate and adaptive immune systems, autophagic dysfunction is also closely related to inflammation, infection, and neurodegeneration. Here we identify that lincRNA-Cox2, previously known as a mediator of both the activation and repression of immune genes expression in innate immune cells, could bind NF-κB p65 and promote its nuclear translocation and transcription, modulating the expression of inflammasome sensor NLRP3 and adaptor ASC...
April 17, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29666186/a-malaria-protein-factor-induces-il-4-production-by-dendritic-cells-via-pi3k-akt-nf-%C3%AE%C2%BAb-signaling-independent-of-myd88-trif-and-promotes-th2-response
#12
Xianzhu Wu, Nagaraj M Gowda, Yuka I Kawasawa, D Channe Gowda
Dendritic cells (DC) and cytokines produced by DC play crucial roles in inducing and regulating pro-/anti-inflammatory and Th1/Th2 responses. DC are known to produce Th1-promoting cytokine, IL-12, in response to malaria and other pathogenic infections, but it is thought that DC do not produce Th2-promoting cytokine, IL-4. Here, we show that a protein factor of malaria parasites induces IL-4 responses by CD11chi MHCIIhi CD3ε- CD49b- CD19- FcεRI- DC via PI3K-Akt-NF-κB signaling independent of TLR-MyD88/TRIF...
April 17, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29664021/a-tlr-akt-foxo3-immune-tolerance-like-pathway-disrupts-the-repair-capacity-of-oligodendrocyte-progenitors
#13
Taasin Srivastava, Parham Diba, Justin M Dean, Fatima Banine, Daniel Shaver, Matthew Hagen, Xi Gong, Weiping Su, Ben Emery, Daniel L Marks, Edward N Harris, Bruce Baggenstoss, Paul H Weigel, Larry S Sherman, Stephen A Back
Cerebral white matter injury (WMI) persistently disrupts myelin regeneration by oligodendrocyte progenitor cells (OPCs). We identified a specific bioactive hyaluronan fragment (bHAf) that downregulates myelin gene expression and chronically blocks OPC maturation and myelination via a tolerance-like mechanism that dysregulates pro-myelination signaling via AKT. Desensitization of AKT occurs via TLR4 but not TLR2 or CD44. OPC differentiation was selectively blocked by bHAf in a maturation-dependent fashion at the late OPC (preOL) stage by a noncanonical TLR4/TRIF pathway that induced persistent activation of the FoxO3 transcription factor downstream of AKT...
May 1, 2018: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29661823/cutting-edge-blockade-of-inhibitor-of-apoptosis-proteins-sensitizes-neutrophils-to-tnf-but-not-lipopolysaccharide-mediated-cell-death-and-il-1%C3%AE-secretion
#14
Kaiwen W Chen, Kate E Lawlor, Jessica B von Pein, Dave Boucher, Motti Gerlic, Ben A Croker, Jelena S Bezbradica, James E Vince, Kate Schroder
The mammalian inhibitor of apoptosis proteins (IAPs) are key regulators of cell death and inflammation. A major function of IAPs is to block the formation of a cell death-inducing complex, termed the ripoptosome, which can trigger caspase-8-dependent apoptosis or caspase-independent necroptosis. Recent studies report that upon TLR4 or TNF receptor 1 (TNFR1) signaling in macrophages, the ripoptosome can also induce NLRP3 inflammasome formation and IL-1β maturation. Whether neutrophils have the capacity to assemble a ripoptosome to induce cell death and inflammasome activation during TLR4 and TNFR1 signaling is unclear...
April 16, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29655569/activation-of-the-porcine-alveolar-macrophages-via-toll-like-receptor-4-nf-%C3%AE%C2%BAb-mediated-pathway-provides-a-mechanism-of-resistin-leading-to-inflammation
#15
Bi Li, Jing Fang, Zhicai Zuo, Sirui Yin, Tingting He, Mingxian Yang, Junliang Deng, Liuhong Shen, Xiaoping Ma, Shumin Yu, Ya Wang, Zhihua Ren, Hengmin Cui
Resistin, a previously discovered cysteine-rich adipokine known to regulate glucose metabolism, has been emerged as a mediator in inflammation and immunity. Its level was supposed to be related to the expression of indicators, such as interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in inflammation. Toll-like receptor 4 (TLR4) was reported to be a receptor for resistin in cells, like leukocytes and peripheral blood mononuclear cells (PBMC). However, the pro-inflammatory role of resistin and its intracellular mechanisms in alveolar macrophages have not been thoroughly validated...
April 11, 2018: Cytokine
https://www.readbyqxmd.com/read/29653364/microrna-20a-protects-human-aortic-endothelial-cells-from-ox-ldl-induced-inflammation-through-targeting-tlr4-and-txnip-signaling
#16
Mantian Chen, Wei Li, Yi Zhang, Jieying Yang
MiR-20a has been previously reported to participate in the development of various human diseases. However, the role of miR-20a in the pathology of atherosclerosis remains elusive. The present study aimed to reveal the relationship between miR-20a expression and atherosclerosis using in vitro cell model. The expression level of miR-20a was detected in human aortic endothelial cells (HAECs) under Ox-LDL exposure. Meanwhile, the regulatory effects of miR-20a on predicted targets (TLR4 and TXNIP) were also determined...
April 10, 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29626604/transgenerational-effects-of-paternal-dietary-astragalus-polysaccharides-on-spleen-immunity-of-broilers
#17
Yulong Li, Xinyu Lei, Zhenchen Yin, Wei Guo, Shengru Wu, Xiaojun Yang
Our previous study indicated that paternal dietary Astragalus polysaccharides (APS) could induce endotoxin tolerance-like response in jejunum of offspring chickens. There exist positive interaction between intestinal mucosal immunity and systemic immunity. So we studied the transgenerational effect and nutri-epigenetic role of paternal dietary APS on spleen immunity. 64 one-day-old Avein breeder cocks were used in a single-factor design with 0 and 10 g/kg APS, respectively, 4 replicated cages each group, and 8 birds each cage...
April 4, 2018: International Journal of Biological Macromolecules
https://www.readbyqxmd.com/read/29610256/myeloid-differentiation-factor-88-myd88-and-il-1r1-signaling-contribute-to-resistance-to-coccidioides-immitis
#18
Suganya Viriyakosol, Lorraine Walls, Sharon Okamoto, Eyal Raz, David L Williams, Joshua Fierer
Rodents are a natural host for the dimorphic pathogenic fungi Coccidioides immitis and posadasii , and mice are a good model for human infection. Humans and rodents both express Dectin-1 and TLR2 on myeloid cells and those receptors collaborate to maximize the cytokine/chemokine responses to spherules (the tissue form of the fungi), and to formalin killed spherules (FKS). We showed that Dectin-1 is necessary for resistance to pulmonary coccidioidomycosis, but the importance of TLR2 in vivo is uncertain. MyD88 is the adapter protein for TLR2 and 4, and IL-1R1 and IL-18R1...
April 2, 2018: Infection and Immunity
https://www.readbyqxmd.com/read/29595418/human-papillomavirus-hpv-16-e6-oncoprotein-targets-the-toll-like-receptor-pathway
#19
Lucas Boeno Oliveira, Ismar R Haga, Luisa Lina Villa
Cervical cancer is one of the leading causes of death in women worldwide and is etiologically linked to human papillomavirus (HPV) infection. Viral early proteins E6 and E7 manipulate cellular functions to promote the virus life cycle and are essential to the cellular transformation process. The innate immune system plays a pivotal role in the natural history of HPV infection. Among the various proteins that mediate the innate immune response, Toll-like receptors (TLRs) recognize pathogen-associated molecular patterns (PAMPs) and initiate the immune response...
March 29, 2018: Journal of General Virology
https://www.readbyqxmd.com/read/29589052/the-nitrone-spin-trap-5-5-dimethyl-1-pyrroline-n-oxide-dampens-lipopolysaccharide-induced-transcriptomic-changes-in-macrophages
#20
M D Muñoz, M C Della Vedova, P R Bushel, D Ganini da Silva, R P Mason, Z Zhai, S E Gomez Mejiba, D C Ramirez
OBJECTIVE: M1-like inflammatory phenotype of macrophages plays a critical role in tissue damage in chronic inflammatory diseases. Previously, we found that the nitrone spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) dampens lipopolysaccharide (LPS)-triggered inflammatory priming of RAW 264.7 cells. Herein, we tested whether DMPO by itself can induce changes in macrophage transcriptome, and that these effects may prevent LPS-induced activation of macrophages. MATERIALS AND METHODS: To test our hypothesis, we performed a transcriptomic and bioinformatics analysis in RAW 264...
March 27, 2018: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
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