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Nathan Goodyear

Lipopolysaccharide activates an innate immune system response in human adipose tissue i... - 0 views

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    Lipopolysaccharide induces innate immune system activation resulting in type II diabetes and obesity.
Nathan Goodyear

Bacterial Lipopolysaccharide-Induced Inflammation Compromises Testicular Function at Mu... - 0 views

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    animal study finds LPS, lipopolysaccharides, decreases Testosterone production at the level of the leydig cells in the testes.
Nathan Goodyear

Bacterial lipopolysaccharide both renders resistant mice susceptible to mercury-induced... - 0 views

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    Lipopolysaccharide, LPS, released from gram negative bacteria exacerbates the innate immune system response to mercury.  This study found increased IgG1 and IgE levels increased in response to Hg with the presence of LPS.   This study looked at the autoimmune impact of LPS in autism.
Nathan Goodyear

Frontiers | Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of... - 0 views

  • lipopolysaccharides (LPS), either alone or in combination, have indicated that when compared, bacterial LPSs exhibit the strongest induction of pro-inflammatory signaling in human neuronal–glial cells in primary coculture of any single inducer, and different LPS extracts from different gastrointestinal (GI)-tract resident Gram-negative bacteria appeared to have different pro-inflammatory potential
  • powerful inducer of the NF-κB
  • In both neocortex and hippocampus, LPS has been detected to range from a ~7- to ~21-fold increase abundance in AD brain
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  • Major Gram-negative bacilli of the human GI-tract, such as the abundant B. fragilis and Escherichia coli (E. coli), are capable of discharging a remarkably complex assortment of pro-inflammatory neurotoxins
  • (i) bacterial amyloids (10, 21); (ii) endotoxins and exotoxins (5, 12); (iii) LPS (12, 18); and (iv) small non-coding RNAs (sncRNAs)
  • integral components of the outer leaflet of the outer membrane of Gram-negative bacteria, LPS
  • LPS, the major molecular component of the outer membrane of Gram-negative bacteria normally serves as a physical barrier providing the bacteria protection from its surroundings
  • LPS is also recognized by the immune system as a marker for the detection of bacterial pathogen invasion and responsible for the development of inflammatory response is perhaps the most potent stimulator and trigger of inflammation known
  • AD-affected brains have remarkably large loads of bacterial-derived toxins compared to controls. The transfer of noxious, pro-inflammatory molecules from the GI-tract microbiome to the CNS may be increasingly important during the course of aging when both the GI-tract and blood–brain barriers become significantly more permeable
  • first evidence of a perinuclear association of LPS with AD brain cell nuclei
  • LPS-mediated stimulation of chronic inflammation, beta-amyloid accumulation, and episodic memory decline in murine models of AD (39, 40) and a biophysical association of LPS with amyloid deposits and blood vessels in human AD patients
  • Strong adherence of LPS to the nuclear periphery has recently been shown to inhibit nuclear maturation and function that may impair or block export of mRNA signals from brain cell nuclei, a highly active organelle with extremely high rates of transcription, mRNA processing, and export into the cytoplasm
  • LPS may be further injurious to the nuclear membrane just as LPS contributes to cerebrovascular endothelial cell membrane injury
  • high intake of dietary fiber is a strong inhibitor of B. fragilis abundance and proliferation in the intact human GI-tract and as such is a potent inhibitor of the neurotoxic B. fragilis-derived amyloids, LPS, enterotoxins, and sncRNAs.
  • GI-tract microbiome-derived LPS may be an important initiator and/or significant contributor to inflammatory degeneration in the AD CNS
  • LPS has been recently localized to the same anatomical regions involved in AD-type neuropathology
  • a known pro-inflammatory transcription factor complex that triggers the expression of pathogenic pathways involved in neurodegenerative inflammation
  • pro-inflammatory amyloids, endo- and exotoxins, LPSs, and sncRNAs but also serve as potent sources of membrane-disrupting agents
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    LPS links gut to inflammation in Alzheimer's disease
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

Lipopolysaccharide Causes an Increase in Intestinal Tight Junction Permeabili... - 0 views

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    LPS increases break in tight junctions, leaky gut, to increase TLR4 expression and signaling.
Nathan Goodyear

Gut Endotoxin Leading to a Decline IN Gonadal function (GELDING) - a novel theory for t... - 0 views

  • GELDING theory (Gut Endotoxin Leading to a Decline IN Gonadal function)
  • trans-mucosal passage of bacterial lipopolysaccharide (LPS) from the gut lumen into the circulation is a key inflammatory trigger underlying male hypogonadism
  • Obesity and a high fat/high calorie diet are both reported to result in changes to gut bacteria and intestinal wall permeability, leading to the passage of bacterial endotoxin (lipopolysaccharide- LPS) from within the gut lumen into the circulation (metabolic endotoxaemia), where it initiates systemic inflammation.
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  • Endotoxin is known to reduce testosterone production by the testis, both by direct inhibition of Leydig cell steroidogenic pathways and indirectly by reducing pituitary LH drive, thereby also leading to a decline in sperm production.
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    Ever heard of the GELDING theory?  This involves the link between LPS endotoxin from the gut and low Testosterone in obese men.
Nathan Goodyear

Metabolic endotoxaemia related inflammation is associated with hypogonadism in overweig... - 0 views

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    Study finds that inflammation that is the result of obesity in men (IL-6) negatively effects the leading cell and Sertoli cells in men.  Testosterone levels in these men correlated significantly with lipopolysaccharide binding protein.  This points to a negative correlation b/t LPS metabolic endotoxemia and low Testosterone.  Could Testosterone merely be the result of an unhealthy diet and gut?
Nathan Goodyear

Laboratory Investigation - Abstract of article: Helicobacter pylori Lipopolysaccharide ... - 0 views

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    H. Pylori produces LPS.  This plays role in the pathogenesis from H. Pylori
Nathan Goodyear

ScienceDirect.com - Zentralblatt für Bakteriologie, Mikrobiologie und Hygiene... - 0 views

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    Borrelia burgdorferi (lyme disease) shown to express LPS, just like dream negative bacteria.
Nathan Goodyear

Targeting gut microbiota in obesity: effects of prebiotics and probiotics : Article : N... - 0 views

  • gut microbes have a role in the host's metabolic homeostasis
  • lipopolysaccharide (LPS)
  • Associations between circulating LPS level, consumption of a high-fat diet and the presence of obesity and type 2 diabetes mellitus have been confirmed in humans
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  • associations have been proposed between high-fat diet, metabolic endotoxemia and levels of inflammatory markers (TLRs and SOCS3) in mononuclear cells
  • A link between energy intake (high-fat diet) and metabolic endotoxemia has also been described
  • high-fat diet induces metabolic endotoxemia in healthy individuals.
  • metabolic endotoxemia is associated with systemic and adipose tissue inflammation in pregnant women with obesity
  • A growing amount of evidence indicates that changes in the integrity of the intestinal barrier occur both in the proximal and the distal part of the gut, which can contribute to the entrance of LPS into the systemic circulation
  • intestinal endocannabinoid system
  • The low-grade systemic inflammation that characterizes the obese phenotype is controlled by peptides that are produced in the gut. These peptides are influenced by the presence or absence of the gut microbiota
  • these findings suggest that the gut microbiota modulates the biological systems that regulate the availability of nutrients, energy storage, fat mass development and inflammation in the host, which are all components of the obese phenotype
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    good look of how the the gut health, or lack there of, can influence energy homeostasis and contribute to obesity.  This article points to the presence of LPS playing a role in metabolic endotoxemia.  It does discuss the importance of the microbiota and their possible role in the low-grade systemic inflammation condition that is obesity.
Nathan Goodyear

Preadipocytes Mediate Lipopolysaccharide-Induced Inflammation and Insulin Resistance in... - 0 views

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    proposed model of how LPS stimulates NF-kappaB activation and the inflammatory cascade.  This plays a key role in the obesity epidemic.
Nathan Goodyear

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

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    only abstract available here.  LPS increased pancreatic cancer cell invasion and progression 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.
Nathan Goodyear

Effects of chronic celecoxib on testicular function in normal and lipopolysaccharide-tr... - 0 views

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    Animal study from '09 found that COX2 inhibitor blunted LPS decrease in testes weight, decrease in testicular interstitial fluid, and serum Testosterone.  The point here is that LPS, in this animal model, decreased gonadal weight and Testosterone production and the anti inflammatory, COX2, blunted that effect.
Nathan Goodyear

Minimal Penetration of Lipopolysaccharide Across the Murine Blood-brain Barrier - 0 views

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    Study finds very small % of LPS actually is able to penetrate BBB, yet based on other studies, this is enough to trigger microglial activation and damage/death to astrocytes and other brain cells.
Nathan Goodyear

Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cel... - 0 views

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    good review of proposed mechanism of how LPS aids in cell death of astrocytes in vivo: LPS damages the endothelium of the BBB, leading to increase permeability.  This exposes astrocytes to LPS directly.  LPS suppressed genetic expression of antioxidant genes.  LPS stimulates cytokine production, including the production of H2O2 from microglial cells in the brain.  An up regulation of iNOS occurs and in the presence of weakened ability to protect against NO and its metabolites occurs.  
Nathan Goodyear

Metformin Inhibits the Production of Reactive Oxygen Species from NADH:Ubiqui... - 0 views

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    Metformin inhibits LPS induced IL-1beta stimulation.  Interesting that metformin is a inhibitor of complex I in the electron transport chain.
Nathan Goodyear

Curcumin Attenuation of Lipopolysaccharide Induced Cardiac Hypertrophy in Rodents - 0 views

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    This is just to cool. Curcumin found to inhibit LPS mediated cardiac hypertrophy. The how is fascinating. No only does LPS induce inflammatory cytokine production, but he inflammation induces disease--cardiac hypertrophy. LPS induces epigenetic changes that lead to the hypertrophy. Curcumin blocked the histone acetylation induced by LPS.
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