TY - JOUR. T1 - Response of amoeboid and ramified microglial cells to lipopolysaccharide injections in postnatal rats - A lectin and ultrastructural study. AU - Wu, C. H.. AU - Wang, H. J.. AU - Wen, C. Y.. AU - Lien, K. C.. AU - Ling, E. A.. PY - 1997/2/2. Y1 - 1997/2/2. N2 - The present study describes the response of amoeboid and ramified microglial cells in the corpus callosum to intraperitoneal lipopolysaccharide injections in postnatal rats as examined by lectin histochemical staining and electron microscopy. In 1 day old rats receiving endotoxin injections and sacrificed at various time intervals, the lectin labelling of amoeboid/ramified microglia was greatly enhanced. The increased labelling persisted in some ramified microglia in rats killed at 14 and 21 days of age; otherwise in normal or control animals of the corresponding stages, the same cells were very weakly stained. In rats killed at 2 days of age after intraperitoneal lipopolysaccharide injection, the number of microglia ...
Incubation of the human U937 histiocytic lymphoma cell line with granulocyte-macrophage colony stimulating factor (GM-CSF) rendered the cells responsive to induction of TNF by LPS. Treatment with IL-6 reduced TNF production in GM-CSF-primed U937 cells. The inhibitory effect was most pronounced (approximately equal to 80%) when IL-6 was added either along with GM-CSF or within the first 3 h of GM-CSF treatment. Both GM-CSF or IL-6 inhibited [3H]TdR uptake in U937 cells, and simultaneous treatment with GM-CSF and IL-6 resulted in an additive inhibitory effect on cell proliferation. However, the inhibition of TNF production could not be explained by the inhibitory effect of IL-6 on cell growth, nor was it due to a reduction in cell viability. An inhibition of TNF production by IL-6 was also demonstrated in cultured human peripheral blood monocytes. Treatment with IL-6 also resulted in a dose-dependent reduction of the 17-kDa TNF band revealed by SDS-PAGE after labeling monocytes with [35S]cysteine ...
The aim of this work was to study the effect of chronic activation of the immune system on the somatotropic axis. Accordingly, the changes in growth hormone (GH) secretion, circulating insulin-like growth factor-I (IGF- I) and IGF binding proteins (IGFBPs) in response to endotoxin lipopolysaccharide (LPS) administration were examined in adult male Wistar rats. Acute LPS injection (2.5, 25 or 250 μg/kg) increased serum corticosterone in a dose-dependent manner and decreased serum levels of insulin and IGF-I, serum GH concentration declined linearly as the LPS dose increased. Western ligand blot showed an increase in the 33 kDa band (corresponding to IGFBP-1 and IGFBP-2) in the rats that received the highest dose of LPS (250 μg/kg). Chronic LPS administration (250 μg/kg daily for 8 days) significantly decreased body weight, serum levels of IGF-I and pituitary GH content, whereas it increased circulating IGFBP-3 (47 kDa band), IGFBP-1 and IGFBP-2 (33 kDa band) and the 24 kDa band (which possibly ...
Ishii, Y; Shinoda, M; and Shikita, M, "Migration inhibitory action of bacterial lipopolysaccharide on progenitor cells of monocyte/macrophage lineage growing in culture in the presence of colony-stimulating factor (csf-1)." (1982). Subject Strain Bibliography 1982. 3652 ...
Bacterial endotoxin lipopolysaccharide (LPS)-induced sepsis is a critical medical condition, characterized by a severe systemic inflammation and rapid loss of muscle mass. Preventive and therapeutic strategies for this complex disease are still lacking. Here, we evaluated the effect of omega-3 (n-3) polyunsaturated fatty acid (PUFA) intervention on LPS-challenged mice with respect to inflammation, body weight and the expression of Toll-like receptor 4 (TLR4) pathway components. LPS administration induced a dramatic loss of body weight within two days. Treatment with n-3 PUFA not only stopped loss of body weight but also gradually reversed it back to baseline levels within one week. Accordingly, the animals treated with n-3 PUFA exhibited markedly lower levels of inflammatory cytokines or markers in plasma and tissues, as well as down-regulation of TLR4 pathway components compared to animals without n-3 PUFA treatment or those treated with omega-6 PUFA. Our data demonstrate that n-3 PUFA intervention
Inflammation of the uterus and oviduct is associated with reduced reproductive performance in humans and domestic animals. Toll-like receptors are expressed in various immune and non-immune cells and play a crucial role in innate immunity. Toll-like receptor e 4 (TLR4) can detect lipopolysaccharide (LPS) from Gram-negative bacteria leading to the secretion of pro-inflammatory cytokines, chemokines, antimicrobial peptides and other inflammatory mediators. To investigate the effects of a local inflammation on the expression levels of TLR4 and pro-inflammatory cytokines, 12 female rabbits received an intracervical infusion with either saline solution endotoxin-free (carrier, 2 mL; n ¼ 6) or LPS (500 mg diluted in 2 mL of saline solution; n ¼ 6). Blood samples were performed at 0, 30, 60 and 90 min and 2,4,6 and 24 h after treatment to evaluate interleukin-1b (IL-1b) and tumor necrosis factor-a (TNF-a) plasma concentrations.. ...
TY - JOUR. T1 - Expression of Gα(i2) mimics several aspects of LPS priming in a murine macrophage-like cell line. AU - Kugi, M.. AU - Kitamura, K.. AU - Cottam, G. L.. AU - Miller, R. T.. PY - 1995/1/1. Y1 - 1995/1/1. N2 - Priming of macrophages with low concentrations of lipopolysaccharide (LPS) enhances the ability of substances that act through heterotrimeric G proteins to stimulate immune cell functions. Although LPS-induced alterations in the expression and functions of G proteins of the α(i) family have been reported in hematopoietic cells, their effects on subsequent steps in LPS priming of macrophages have not been defined. To study the role of Gα(i2) in priming of macrophages by LPS, we expressed a mutant, activated form of α(i2) (α(i2Q2051)) in P388D1 cells, and compared its effects on PAF-dependent Ca signalling and arachidonic acid release to those in cells treated with LPS. In control P388D1 cells, treatment with LPS (100 ng/ml) for 1 hr increased the amount of α(i2) protein ...
Angiotensin II (ANG II) has been shown to have proinflammatory properties. To investigate whether ANG II is involved in the lipopolysaccharide (LPS)-induced production of a pyrogenic/proinflammatory cytokine, interleukin-6 (IL-6), we examined the effects of an angiotensin-converting-enzyme (ACE) inhibitor, lisinopril, on LPS-induced fever and on the expression of IL-6 mRNA in the spleen of dehydrated rats (in which the secretion of ANG II increases). The results showed that the ACE inhibitor significantly inhibited LPS-induced fever as well as the splenic expression of IL-6 mRNA in dehydrated rats. It is suggested that endogenous ANG II may be involved in the production of IL-6 that occurs in response to LPS, and thereby contribute to the LPS-induced febrile response in dehydrated rats ...
TY - JOUR. T1 - Inhibition of LPS-induced C/EBPδ by trichostatin A has a positive effect on LPS-induced cyclooxygenase 2 expression in RAW264.7 cells. AU - Liu, Yi Wen. AU - Wang, Shao An. AU - Hsu, Tsung Yi. AU - Chen, Tsu An. AU - Chang, Wen Chang. AU - Hung, Jan Jong. PY - 2010/8/15. Y1 - 2010/8/15. N2 - Cyclooxygenase 2 (COX-2) is an important inflammatory factor. Previous studies have indicated that COX-2 is induced with lipopolysaccharide (LPS) treatment. Here, we found that an inhibitor of histone deacetylase (HDAC), trichostatin A (TSA), cannot repress LPS-induced COX-2 but it increased the COX-2 level in RAW264.7 cells. We found no significant difference in NF-κB activation and ERK1/2 phosphorylation, but LPS-induced C/EBPδ expression was completely abolished after TSA treatment of LPS-treated cells. Interesting, reporter assay of C/EBPδ promoter revealed that Sp1-binding site is important. Although there was no alteration in c-Jun levels, but the phosphorylation of c-Jun at its ...
This project established an in vivo method to identify and manipulate expression of markers of osteoarthritis (OA). Specifically, strategies that predictably induce joint inflammation to evaluate dietary methods of OA prevention in young horses have yet to be accomplished. Therefore, the 3 studies described herein were conducted to determine effectiveness of an intra-articular lipopolysaccharide (LPS) challenge on markers of inflammation and cartilage metabolism in young horses and potential of dietary glucosamine hydrochloride (HCl) to mitigate these alterations. In the first study, horses were challenged with 0.25 ng or 0.50 ng of intra-articular LPS solution or lactated ringers solution (control). Injection of LPS increased inflammation based on synovial prostaglandin E2 (PGE2) concentrations. Carboxypeptide of type II collagen (CPII), a maker of type II collagen synthesis, also increased in a dose-dependent manner. However, clinical parameters of health were not influenced and remained ...
We recently showed that lipopolysaccharide (LPS) is a potent inducer of interleukin-8 (IL-8) expression in human polymorphonuclear leucocytes (PMN), at the level of both mRNA and protein, and that interferon-gamma (IFN gamma) inhibits IL-8 mRNA accumulation in stimulated PMN. To further define the molecular basis of the regulation of IL-8 gene expression in PMN, we investigated the effects of LPS and IFN gamma at both the transcriptional and post-transcriptional levels. As determined by Northern blot analysis, new protein synthesis was not required for the induction of IL-8 mRNA expression by LPS. Neither did the half-life of IL-8 mRNA in LPS-treated PMN differ from that observed in untreated cells. However, nuclear run-on analysis revealed that LPS increased the transcription of the IL-8 and IL-1 beta genes and that, in LPS-activated cells, IFN gamma markedly inhibited the rate of IL-8 gene transcription, but not that of IL-1 beta. IFN gamma did not affect IL-8 mRNA stability in LPS-treated ...
Human CD34+ Progenitor Cells Freshly Isolated from Umbilical Cord Blood Attenuate Inflammatory Lung Injury following Lipopolysaccharide Challenge
TY - JOUR. T1 - IFN-γ/lipopolysaccharide activation of macrophages is associated with protein kinase C-dependent down-modulation of the colony-stimulating factor-1 receptor. AU - Baccarini, M.. AU - Sbarba, P. D.. AU - Buscher, D.. AU - Bartocci, A.. AU - Stanley, E. R.. PY - 1992/1/1. Y1 - 1992/1/1. N2 - IFNγ/LPS treatment increases macrophage tumoricidal and microbicidal activity and inhibits CSF-1-induced macrophage proliferation. The mechanism underlying the latter effect was investigated in the CSF-1-dependent mouse macrophage cell line, BAC-1.2F5. IFN-γ and LPS together dramatically reduced the total number of CSF-1 receptors (CSF-1R) via selective degradation of the cell surface form. Processing and transport of intracellular CSF-1R to the cell surface were unaffected. IFN-γ alone had no effect but significantly enhanced LPS-induced CSF-1R down-regulation. The reduction in CSF-1R number was protein kinase C-dependent and involved changes in serine phosphorylation of the receptor at ...
Macrophages activated by the Gram-negative bacterial product lipopolysaccharide switch their core metabolism from oxidative phosphorylation to glycolysis. Here we show that inhibition of glycolysis with 2-deoxyglucose suppresses lipopolysaccharide-induced interleukin-1β but not tumour-necrosis factor-α in mouse macrophages. A comprehensive metabolic map of lipopolysaccharide-activated macrophages shows upregulation of glycolytic and downregulation of mitochondrial genes, which correlates directly with the expression profiles of altered metabolites. Lipopolysaccharide strongly increases the levels of the tricarboxylic-acid cycle intermediate succinate. Glutamine-dependent anerplerosis is the principal source of succinate, although the GABA (γ-aminobutyric acid) shunt pathway also has a role. Lipopolysaccharide-induced succinate stabilizes hypoxia-inducible factor-1α, an effect that is inhibited by 2-deoxyglucose, with interleukin-1β as an important target. Lipopolysaccharide also increases ...
The pathophysiology of acute lung injury (ALI) differs according to the type of insult. We hypothesized that the administration route of bone marrow-derived mononuclear cell (BMDMC) therapy might have different effects on lung and distal organs in models of pulmonary (p) or extrapulmonary (exp) ALI. Forty-eight C57BL/6 mice: 36 females and 12 males (20-25 g) were used. In control animals, sterile saline solution was intratracheally or intraperitoneally injected. whereas ALI animals received Escherichia coli lipopolysaccharide intratracheally (40 μg, ALIp) or intraperitoneally (400 μg, ALIexp). Six hours after lipopolysaccharide administration, ALIp and ALIexp animals were further randomized into subgroups receiving saline or BMDMC (2×106) intravenously (BMDMC iv) or intratracheally (BMDMC it). At day 7: 1) BMDMC iv and it decreased static elastance, alveolar collapse, collagen fiber content, and bronchoalveolar lavage fluid cellularity; 2) BMDMC it increased the number of green fluorescent ...
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Tetracyclines downregulate the production of LPS-induced cytokines and chemokines in THP-1 cells via ERK, p38, and nuclear factor-κB signaling pathwaysTetracyclines downregulate the production of LPS-induced cytokines and chemokines in THP-1 cells via ERK, p38, and nuclear factor-κB signaling pathways ...
Lipid-containing polysaccharides which are endotoxins and important group-specific antigens. They are often derived from the cell wall of gram-negative bacteria and induce immunoglobulin secretion. The lipopolysaccharide molecule consists of three parts: LIPID A, core polysaccharide, and O-specific chains (O ANTIGENS). When derived from Escherichia coli, lipopolysaccharides serve as polyclonal B-cell mitogens commonly used in laboratory immunology. (From Dorland, 28th ed ...
Lafleur, L, "Lipopolysaccharide induction of immunoglobulin synthesis in irradiated lymphocytes." (1978). Subject Strain Bibliography 1978. 4335 ...
TY - JOUR. T1 - L-Arginine attenuates lipopolysaccharide-induced lung chemokine production. AU - Calkins, Casey M.. AU - Bensard, Denis D.. AU - Heimbach, Julie K.. AU - Meng, Xianzhong. AU - Shames, Brian D.. AU - Pulido, Edward J.. AU - McIntyre, Robert C.. PY - 2001/3. Y1 - 2001/3. N2 - Chemokines stimulate the influx of leukocytes into tissues. Their production is regulated by nuclear factor-κB (NF-κB), an inducible transcription factor under the control of inhibitory factor κB-α (IκB-α). We have previously demonstrated that L-arginine (L-Arg) attenuates neutrophil accumulation and pulmonary vascular injury after administration of lipopolysaccharide (LPS). We hypothesized that L-Arg would attenuate the production of lung chemokines by stabilizing IκB-α and preventing NF-κB DNA binding. We examined the effect of L-Arg on chemokine production, IκB-α degradation, and NF-κB DNA binding in the lung after systemic LPS. To block nitric oxide (NO) production, a NO synthase inhibitor was ...
MAB526Ge22, Monoclonal Antibody to Lipopolysaccharide (LPS), LOS; Lipoglycans; Lipooligosaccharide; Lipo-Oligosaccharide; Endotoxin | Products for research use only!
CD14 is a 55 kDa GPI-anchored glycoprotein, constitutively expressed on the surface of mature monocytes, macrophages, and neutrophils, where serves as a multifunctional lipopolysaccharide receptor; it is also released to the serum both as a secreted and enzymatically cleaved GPI-anchored form. CD14 binds lipopolysaccharide molecule in a reaction catalyzed by lipopolysaccharide-binding protein (LBP), an acute phase serum protein. The soluble sCD14 is able to discriminate slight structural differences between lipopolysaccharides and is important for neutralization of serum allochthonous lipopolysaccharides by reconstituted lipoprotein particles. CD14 affects allergic, inflammatory and infectious processes ...
The P2X(7) receptor (P2X(7)R) is an ATP-gated ion channel expressed by monocytes and macrophages. To directly address the role of this receptor in interleukin (IL)-1 beta post-translational processing, we have generated a P2X(7)R-deficient mouse line. P2X(7)R(-/-) macrophages respond to lipopolysaccharide and produce levels of cyclooxygenase-2 and pro-IL-1 beta comparable with those generated by wild-type cells. In response to ATP, however, pro-IL-1 beta produced by the P2X(7)R(-/-) cells is not externalized or activated by caspase-1. Nigericin, an alternate secretion stimulus, promotes release of 17-kDa IL-1 beta from P2X(7)R(-/-) macrophages. In response to in vivo lipopolysaccharide injection, both wild-type and P2X(7)R(-/-) animals display increases in peritoneal lavage IL-6 levels but no detectable IL-1. Subsequent ATP injection to wild-type animals promotes an increase in IL-1, which in turn leads to additional IL-6 production; similar increases did not occur in ATP-treated, LPS-primed ...
Data_Sheet_1_K5 Capsule and Lipopolysaccharide Are Important in Resistance to T4 Phage Attack in Probiotic E. coli Strain Nissle 1917.pdf
Ex vivo LPS stimulation of whole blood will be a good alternative challenge to induce an inflammatory response and examine differences in the inflammatory response between healthy and compromised subjects.. The purpose of the current study is to examine the inflammatory response in a younger population (35-45 yrs old) to see whether in this population also differences in the ex vivo LPS induced cytokine response exists between healthy and compromised subjects, as is seen in elderly subjects. Overweight subjects showing a state of disturbed blood glucose control will be included as subjects with compromised health and compared to healthy lean subjects with the same age (shifting from healthy towards unhealthy, not diseased).. Hypothesis Ex vivo LPS stimulation of whole blood will induce a measurable inflammatory cytokine response in a healthy population that is different from a response of the compromised population. The investigators will include subjects aged 35-45 years that differ in health ...
Sigma-Aldrich offers abstracts and full-text articles by [Agnieszka Pladzyk, Aramati B M Reddy, Umesh C S Yadav, Ravinder Tammali, Kota V Ramana, Satish K Srivastava].
Lipopolysaccaride (LPS) is one of the main components of the Gram negative cell wall, it gets released into the blood stream when bacterial cell are destroyed or lysed by the immune system. If the levels are allowed to build up it can cause sepsis, which is potentially life threatening. CD14 is a cell surface protein which is capable of binding LPS and setting off a series of reaction to neutralise it. In this experiment three types of cells, THP-1 Monocytes, differentiated THP Macrophages and MM6 Monocytes, where incubated with 5 different strain of LPS, there were also two incubation periods. The levels of membrane bound CD14 were measured by binding with monoclonal antibodies conjugated with a fluorochrome. The samples where then read by a flow cytometer in order to determine the change in CD14 levels from no LPS to incubated samples. The soluble CD14 was measured by ELISA and the results were read by a plate reader and then analysed in comparison to known standards in order to determine the ...
Clinical depression is frequently comorbid with chronic inflammatory disease, and neuroinflammation is currently proposed as a key mechanism in major depressive disorders. Different from unpredictable chronic stress, which is a well-established animal model for depression, predictable chronic mild stress (PCMS), a routine stress experienced in day-to-day life, has been demonstrated to improve mood and memory. In the present study, we assess the effects of PCMS (5 min of daily restrain stress for 4 weeks) on depressive-like behavior, neuroinflammation, oxidative stress, and pyrin domain containing three (NLRP3) activation in hippocampus of mice subjected to peripheral immune challenge by lipopolysaccharide (LPS). We found that PCMS facilitated the recovery from LPS-induced depressive- or anxiety-like behavior. Concurrent with the reversal of abnormal behavioral changes, PCMS suppressed LPS-induced proinflammatory cytokine expression, microglia activation, and oxidative stress in hippocampus.
5 (5-LO) takes on a pivotal part in the progression of atherosclerosis. Moreover the LPS-enhanced phosphorylation of Akt was significantly attenuated in cells pretreated with an anti-TLR4 antibody. Taken together 5 expression in LPS-stimulated monocytes is regulated at the transcriptional level via TLR4/Akt-mediated activations of Sp1 and NF-κB pathways in monocytes. Keywords: Akt Atherosclerosis LPS Monocytes 5 INTRODUCTION Monocytes play a central role in several pathophysiological conditions when the progression of cardiovascular disease stems from underlying inflammatory reactions [1 2 Lipopolysaccharide (LPS) is a glycolipid component of the gram-negative bacterial cell wall and a major inflammatory cytokine that induces inflammatory responses by activating monocytes [3 4 5 and 5-lipoxygenase (5-LO) is a potent proinflammatory Solithromycin mediator in several inflammatory diseases including atherosclerosis [6 7 8 However mechanisms responsible for the LPS-induced expression of 5-LO in ...
Tempest-Roe, S, Tam, FW and Taylor, SRJ (2013) The duration of LPS priming determines the phenotype of macrophage, but not T cell P2X7 responses In: British Society of Immunology Annual Congress, 2013-12-02 - ?. Full text not available from this repository ...
Neuroinflammation, characterized by chronic activation of the myeloid-derived microglia, is a hallmark of Alzheimers disease (AD). Systemic inflammation, typically resulting from infection, has been linked to the progression of AD due to exacerbation of the chronic microglial reaction. However, the mechanism and the consequences of this exacerbation are largely unknown. Here, we mimicked systemic inflammation in AD with weekly intraperitoneal (i.p.) injections of APPSWE/PS1ΔE9 transgenic mice with E. coli lipopolysaccharide (LPS) from 9 to 12 months of age, corresponding to the period with the steepest increase in amyloid pathology. We found that the repeated LPS injections ameliorated amyloid pathology in the neocortex while increasing the neuroinflammatory reaction. To elucidate mechanisms, we analyzed the proteome of the hippocampus from the same mice as well as in unique samples of CNS myeloid cells. The repeated LPS injections stimulated protein pathways of the complement system, retinoid
Characterization of diffusing capacity and perfusion of the rat lung in a lipopolysaccaride disease model using hyperpolarized 129Xe.
We have recently shown that lipopolysaccharide (LPS)-binding protein (LBP) is a lipid transfer protein that catalyzes two distinct reactions: movement of bacterial LPS (endotoxin) from LPS micelles to soluble CD14 (sCD14) and movement of LPS from micelles to reconstituted high density lipoprotein (R-HDL) particles. Here we show that LBP facilitates a third lipid transfer reaction: movement of LPS from LPS-sCD14 complexes to R-HDL particles. This action of LBP is catalytic, with one molecule of LBP enabling the movement of multiple LPS molecules into R-HDL. LBP-catalyzed movement of LPS from LPS-sCD14 complexes to R-HDL neutralizes the capacity of LPS to stimulate polymorphonuclear leukocytes. Our findings show that LPS may be transferred to R-HDL either by the direct action of LBP or by a two-step reaction in which LPS is first transferred to sCD14 and subsequently to R-HDL. We have observed that the two-step pathway of LPS transfer to R-HDL is strongly favored over direct transfer. ...
Introduction: We have previously reported that bacterial toxins, especially endotoxins such as lipopolysaccharides (LPS), might be important causative agents in the pathogenesis of rheumatoid arthritis (RA) in an in vitro model that simulates the potential effects of residing in damp buildings. Since numerous inflammatory processes are linked with the nuclear factor-kappa B (NF-kappa B), we investigated in detail the effects of LPS on the NF-kappa B pathway and the postulated formation of procollagen-endotoxin complexes. Methods: An in vitro model of human chondrocytes was used to investigate LPS-mediated inflammatory signaling. Results: Immunoelectron microscopy revealed that LPS physically interact with collagen type II in the extracellular matrix (ECM) and anti-collagen type II significantly reduced this interaction. BMS-345541 (a specific inhibitor of I kappa B kinase (IKK)) or wortmannin (a specific inhibitor of phosphatidylinositol 3-kinase (PI-3K)) inhibited the LPS-induced degradation of ...
The NF-kB pathway is vital for immune system regu- lation and pro-inflammatory signaling. Many disor- ders and diseases, including cancer, can be linked to NF-kB dysregulation. When macrophages recognize the presence of a pathogen, the signaling pathway is activated - resulting in the nuclear translocation of NF- kB to turn on pro-inflammatory genes. Here, we demonstrate the effects of a novel microtubule depol- ymerizer, NT-07-16, a polysubstituted pyrrole on this process. Treatment with NT-07-16 decreased the pro- duction of pro-inflammatory mediators in a dose-de- pendent manner in RAW264.7 mouse macrophages. It appears that the reduction in pro-inflammatory me- diators by the macrophages after exposure to NT-07- 16 may be due to a decrease in the translocation of NF- κB into the nucleus. Therefore, this study suggests that, upon activation of mouse macrophages, NF-kB translocates into the nucleus by way of the microtu- bule network and that disruption of this network by NT-07-16 reduces the
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I have done LPS extraction using the hot phenol-water method which was originally decribed by Westphal, O. & Jann, K. (1965) Bacterial lipopolysaccharides: extraction with phenol-water and further applications of the procedure. Methods Carbohydr Chem 5: 83-91. I used a modification of it to extract Neisseria gonorrhoeae LPS (Mol Microbiol 2001 42: 167) which worked pretty well. If you need a more detailed protocol I could send you that ...
Airway exposure of lipopolysaccharide (LPS) is shown to regulate type I and type II helper T cell induced asthma. While high doses of LPS derive Th1- or Th17-immune responses, low LPS levels lead to Th2 responses. In this paper, we analyze a mathematical model of Th1/Th2/Th17 asthma regulation suggested by Lee (S. Lee, H.J. Hwang, and Y. Kim, Modeling the role of TGF-$\beta$ in regulation of the Th17 phenotype in the LPS-driven immune system, Bull Math Biol., 76 (5), 1045-1080, 2014) and show that the system can undergo a Hopf bifurcation at a steady state of the Th17 phenotype for high LPS levels in the presence of time delays in inhibition pathways of two key regulators: IL-4/Th2 activities ($H$) and TGF-$\beta$ levels ($G$). The time delays affect the phenotypic switches among the Th1, Th2, and Th17 phenotypes in response to time-dependent LPS doses via nonlinear crosstalk between $H$ and $G$. An extended reaction-diffusion model also predicts coexistence of these phenotypes under various ...
The bacterial lipopolysaccharide also known as endotoxin is exhaustively covered in the present work. Central emphasis is placed upon the fine chemical structure of the lipopolysaccharide and its sign
... : Expression of the iNOS and Arg1 genes in BMA cells as indicators of their polarization states following treatment with LPS, IFNγ+LPS or IL-4. Transcriptional expression of genetic markers in BMA macrophages was determined following treatment and analyzed by densitometry. A. Expression of iNOS was found to increase following LPS and IFNγ+LPS treatments, respectively. Treatment with IL-4 reduced iNOS expression. B. Arg1 expression was found to decrease following LPS treatment, while treatment with IFNγ+LPS and IL-4 produced increased it, with IL-4-treated cells having higher expression than IFNγ+LPS-treated BMAs. This is one representative experiment from 5 independent trials ...
Although COX-1 mRNA and protein expression are detectable in normal brain tissue (Ivanov et al., 2002; Aid et al., 2008), we are unaware of previous evidence for cerebrovascular enzyme expression under basal or endotoxin-stimulated conditions. Our findings thus seem to challenge evidence that brain COX-1 is insensitive to proinflammatory challenges (Ivanov and Romanovsky, 2004). This apparent disparity may be explained by the fact that COX-1 is normally expressed principally by parenchymal (microglial) cells that may be LPS unresponsive but that could serve to dilute regulatory effects on vascular enzyme expression. Our failure to detect LPS effects on COX-1-IR in brain homogenates is consistent with this view.. Previous evidence supporting COX-1 localization to CNS vascular or glial cells has been gathered primarily in injury or disease models. Accumulation of COX-1-expressing macrophages and upregulation by ECs and microglia has been reported after spinal injury in rats (Schwab et al., 2000a) ...
Effects of NCTS on LPS-induced production of NO2− in the cell supernatants and intracellular NO formation in RAW264.7 macrophages. Cells were treated with LPS
Human in vivo models of systemic inflammation are used to study the physiological mechanisms of inflammation and the effect of drugs and nutrition on the imm...
A large body of evidence suggests that atherosclerosis is an inflammatory disease, in which cytokines and growth factors play a major role in disease progression. The methanolic extracts of Sphaeranthus indicus as well as its active ingredient, 7-hydroxy frullanoide (7-HF), are shown to suppress LPS-induced cytokine production from mononuclear cells, and inhibit the expression of VCAM1, ICAM1 and E-selectin by TNF-α- stimulated HUVECs in a concentration-dependent manner. We tested the hypothesis that the inhibition of cytokines and adhesion molecules should attenuate the progression of atherosclerosis, independent of changes in the lipid profile. Studies were carried out in two animal models: a high fat-fed LDLr-/- mouse and a high fat-fed hyperlipidemic hamster. Methanolic extract of S. indicus was dosed to hyperlipidemic LDLr-/- at 100 and 300 mg (equivalent to 20 and 60 mg 7-HF)/kg body weight/ day for 8 weeks, and plasma lipids as well as aortic lesion area were quantitated. Hyperlipidemic hamsters
A large body of evidence suggests that atherosclerosis is an inflammatory disease, in which cytokines and growth factors play a major role in disease progression. The methanolic extracts of Sphaeranthus indicus as well as its active ingredient, 7-hydroxy frullanoide (7-HF), are shown to suppress LPS-induced cytokine production from mononuclear cells, and inhibit the expression of VCAM1, ICAM1 and E-selectin by TNF-α- stimulated HUVECs in a concentration-dependent manner. We tested the hypothesis that the inhibition of cytokines and adhesion molecules should attenuate the progression of atherosclerosis, independent of changes in the lipid profile. Studies were carried out in two animal models: a high fat-fed LDLr-/- mouse and a high fat-fed hyperlipidemic hamster. Methanolic extract of S. indicus was dosed to hyperlipidemic LDLr-/- at 100 and 300 mg (equivalent to 20 and 60 mg 7-HF)/kg body weight/ day for 8 weeks, and plasma lipids as well as aortic lesion area were quantitated. Hyperlipidemic hamsters
CEB526Ge, ELISA Kit for Lipopolysaccharide (LPS), 脂多糖(LPS)检测试剂盒(酶联免疫吸附试验法), LOS; Lipoglycans; Lipooligosaccharide; Lipo-Oligosaccharide; Endotoxin | 仅供体外研究使用,不用于临床诊断!请索取进口关税税单及报关单!
The inheritance of B-cell responsiveness to lipopolysaccharide (LPS) was studied in 55 crosses between mice of the low-responder strain C3H/HeJ and the high-responder strains B10.5M and C3H/Tif. F1 hybrid mice between the low-and the high-responder strains, showed in every case responses which were intermediate between the responses obtained with each parent. The responsiveness among F2 hybrid and backcross mice to either high- or low-responder parents, segregated into intermediate, high, or low categories, respectively. The present results are compatible with the hypothesis that responsiveness to LPS is determined by one single, codominantly expressed, autosomal gene. The capacity to develop a specific thymus-independent response to a hapten-LPS conjugate, also under genetical control, was found to segregate together with the capacity to develop polyclonal responses to LPS. ...
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Kirkland, T. N., Ziegler, E. J., Tobias, P., Ward, D. C., Michalek, S. M., McGhee, J. R., Macher, I., Urayama, K., Appelmelk, B. J. Inhibition of lipopolysaccharide activation of 70z/3 cells by anti-lipopolysaccharide antibodies Journal of Immunology 1988 141:3208-3213 PMID:3262686 ...
2XCI: Structural and Mechanistic Analysis of the Membrane-Embedded Glycosyltransferase Waaa Required for Lipopolysaccharide Synthesis.