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Nathan Goodyear

Lipopolysaccharide (LPS) increases the invasive ability of pancreatic cancer cells thro... - 0 views

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    Lipopolysaccharide (LPS) activates Toll-like 4 receptors (TLR-4) to increase cancer invasion, growth, and metastasis.
Nathan Goodyear

Elevated Muscle TLR4 Expression and Metabolic Endotoxemia in Human Aging - 0 views

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    Not a direct cause and effect, but a clear associated between metabolic endotoxemia and increase in TLR4
Nathan Goodyear

A TRIFfic Perspective on Acute Lung Injury: Cell - 0 views

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    Recognition of TLR4 PRR involvement in cytokine storm from SARS all the way back to 2008. Md88 and TRIF involved.
Nathan Goodyear

Minireview: Inflammation and Obesity Pathogenesis: The Hypothalamus Heats Up - 0 views

  • Leptin, secreted by adipocytes in proportion to body fat mass
  • The saturated fatty acid palmitate (16:0) induces NF-κB signaling through a TLR4-dependent mechanism
  • 18:0 (stearic) and longer saturated fatty acids as well as linolenic acid (18:3) increased proinflammatory cytokines, ER stress markers, and TLR4 activation
  • ...6 more annotations...
  • (SOCS)-3. A member of a protein family originally characterized as negative feedback regulators of inflammation (13, 37), SOCS3 inhibits insulin and leptin signaling
  • IKKβ signaling in discrete neuronal subsets appears to be required for both hypothalamic inflammation and excess weight gain to occur during HF feeding
  • the paradoxical observation that hyperphagia and weight gain occur when hypothalamic inflammation is induced by HF feeding, yet when it occurs in response to systemic or local inflammatory processes (e.g. administration of endotoxin), anorexia and weight loss are the rule
  • , serves as a circulating signal of energy stores in part by providing feedback inhibition of hypothalamic orexigenic pathways [e.g. neurons that express neuropeptide Y and agouti-related peptide (AgRP)]
  • and stimulating anorexigenic neurons
  • signals from Toll-like receptors (TLRs), evolutionarily conserved pattern recognition molecules critical for detecting pathogens, amplified through signaling intermediates such as MyD88 activate the inhibitor of κB-kinase-β (IKKβ)/nuclear factor-κB (NF-κB), c-Jun N-terminal kinase (Jnk) and other intracellular inflammatory signals in response to stimulation by circulating saturated fatty acids
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    great read on the current understanding of how obesity and resultant inflammation disrupts hypothalamic function.
Nathan Goodyear

Histochemistry and Cell Biology, Volume 127, Number 2 - SpringerLink - 0 views

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    Abstract only, but this study shows that the innate immunity plays a role in the development of obesity through the TLR.  LPS was shown to stimulate the inflammatory cascade through the TLRs
Nathan Goodyear

TLR Signaling in the Gut in Health and Disease - 0 views

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    How the gut contributes to inflammation and disease: through TLR.
Nathan Goodyear

The intestinal epithelial barrier: how to dist... [Semin Immunol. 2007] - PubMed - NCBI - 0 views

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    TLRs and NODs play important role in GI mucosal immunity.
Nathan Goodyear

BACTERIAL INTERACTIONS WITH CELLS OF THE INTESTINAL MUCOSA: TOLL-LIKE RECEPTORS AND NOD... - 0 views

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    How interactions between the bacteria, both commensal and pathogenic, occur.  This can precipitate disease or promote health.  This occurs through TLRs and Nods
Nathan Goodyear

Benign prostatic hyperplasia: a new meta... [J Endocrinol Invest. 2014] - PubMed - NCBI - 0 views

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    The authors of this paper describe BPH as a metabolic disease: involving inflammation with increased expression of TLRs, hormone imbalance and altered metabolism
Nathan Goodyear

High expression of Toll-like receptor 4/myeloid differentiation factor 88 signals corre... - 0 views

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    High TLR4 and MyD88 expression on the surface of colorectal cancer cells associated with increase liver mets potential and worsened prognosis.  LPS works through TLR4 and MyD88.
Nathan Goodyear

Lipopolysaccharide-induced toll-like receptor 4 signaling enhances the migratory abilit... - 0 views

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    LPS stimulation induced increased mets potential in esophageal cell culture study.
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