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Results for “ENDOTOXINS”

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At least 361 records · Page 20Linked to original sources
PubMed1996

Effect of heat shock and endotoxin stress on enterocyte viability apoptosis and function varies based on whether the cells are exposed to heat shock or endotoxin first.

BACKGROUND: Stress-gene responses, including the heat shock (HS) response and the acute phase response, are protective mechanisms for cells after exposure to stress. Both responses cannot occur simultaneously, and, in endothelial cells, the sequence of stress-gene expression seems to be a critical factor in whether cellular protection or injury occurs. OBJECTIVE: To determine if the sequence of stress-gene expression affects cellular protection or injury in epithelial cells. DESIGN: Randomized controlled in vitro study. SETTING: University research laboratory. SUBJECTS: Rat intestinal epithelial cell-6 (IEC-6) cells were grown on 35-mm culture dishes, chamber slides, or in a bicameral system to confluence or until tight junction integrity was established. INTERVENTIONS: Rat IEC-6 cells were examined for viability, apoptosis, and bacterial translocation (BT) after exposure to 25-micrograms/mL lipopolysaccharide (LPS) for 18 hours to HS (43 degrees C) for 90 minutes, to LPS followed by HS, or to HS followed by LPS. MAIN OUTCOME MEASURES: The IEC-6 cells were stained for viability and apoptosis using trypan blue and a direct immunoperoxidase detection of digoxigenin-labeled genomic DNA (Apop Tag Plus In Situ Apoptosis Detection Kit, Oncor, Gaithersburg, Md), respectively. Bacterial translocation was measured by culturing the bacteria (ie, Escherichia coli) that crossed the IEC-6 cell monolayer in the bicameral system. RESULTS: Control cells (medium only) and cells exposed to LPS alone, HS alone, or HS followed by LPS had a viability from 92% to 98%, and the percentage of apoptotic cells ranged from 2.2% to 5.7%. In contrast, IEC-6 cells exposed to LPS followed by HS had a significantly lower viability (83%, P < .05 vs all other groups) and a higher percentage of apoptotic cells (12.2%, P < .01). At 3 hours after challenge with E coli, the LPS-exposed IEC-6 cell monolayers had significantly increased BT vs control monolayers (P < .05), while the IEC-6 cell monolayers exposed to HS followed by LPS had decreased BT (P < .05). Conversely, cells exposed to LPS followed by HS had the highest magnitude of BT (P < .01 vs all other groups). CONCLUSIONS: These results indicate that preinduction of HS response can diminish LPS-induced cell injury, while induction of HS response after the LPS challenge (ie, the acute phase response) may lead to decreased enterocyte viability, increased apoptosis, and cellular dysfunction as manifested by BT.

Acute-Phase Reaction↗
PubMed2003

Evidence of expression of endotoxin receptors CD14, toll-like receptors TLR4 and TLR2 and associated molecule MD-2 and of sensitivity to endotoxin (LPS) in islet beta cells.

CD14, a GPI-linked membrane protein, is a component of the lipopolysaccharide (LPS) receptor complex, one of the pattern-recognizing receptors (PRR) expressed by myeloid lineage cells. Here we report that CD14, the functionally linked toll-like receptor molecules, TLR2 and TLR4, and the associated molecule MD-2 are expressed in endocrine cells of the human pancreatic islets. CD14 expression in human pancreatic islets was determined by immunofluorescence staining of tissue sections and primary cultures, and confirmed by flow cytometry of dispersed normal islets and SV40-transformed islet cells (HP62). The latter cells synthesized and secreted CD14 in response to lipopolysaccharide (LPS) in a time- and dose-dependent manner. Reverse transcription polymerase chain reaction (RT-PCR)-Southern was positive for CD14, TLR2, TLR4 and MD-2 in human pancreas, purified islets and HP62 cells. In vitro experiments using rat islets (also positive for CD14 by RT-PCR) and HP62 cells showed that LPS regulates glucose-dependent insulin secretion and induces inflammatory cytokines [interleukin (IL)-1alpha, IL-6 and tumour necrosis factor (TNF)-alpha]. The functional expression of CD14 and associated molecules in islet beta cells adds a new pathway that islet cells may follow to adjust their function to endotoxaemia situations and become vulnerable to the inflammatory events that occur during diabetogenic insulitis.

Adolescent↗
PubMed1996

Changes in endotoxin-induced cytokine production by whole blood after in vivo exposure of normal humans to endotoxin.

Whole blood of 6 healthy subjects, who were intravenously injected with lipopolysaccharide (LPS, 2 ng/kg), was stimulated ex vivo with LPS (10 ng/mL). Three and 6 h after injection of LPS, whole blood produced less tumor necrosis factor-alpha (TNF), interleukin (IL)-1beta, IL-6, and IL-10 (all P < .05). By contrast, the production of IL-1 receptor antagonist was enhanced after LPS injection (P < .05). Plasma obtained 2 h, but not 1 h, after in vivo administration of LPS showed a dose-dependent inhibition of TNF, IL-1beta, and IL-6 production by LPS-stimulated whole blood from 6 other healthy donors not previously exposed to LPS, while the production of IL-10 and IL-1 receptor antagonist were not or were marginally influenced. LPS tolerance represents a purposeful adaptation of the host, rather than a generalized hyporesponsiveness, and is at least partly mediated by soluble factors produced within 2 h after previous exposure to LPS.

Adult↗
PubMed1997

Notoginsenoside R1 counteracts endotoxin-induced activation of endothelial cells in vitro and endotoxin-induced lethality in mice in vivo.

In this study we investigated a possible counteracting activity notoginsenoside R1 (NG-R1) on lipopolysaccharide (LPS)-induced effects in vitro and in vivo. The upregulation of plasminogen activator inhibitor-1 (PAI-1) antigen due to LPS (1 microgram/mL for 12 hours) in human umbilical vein endothelial cells (HUVECs) was prevented when the cells were incubated simultaneously with 100 micrograms/mL NG-R1 (PAI-1 antigen: LPS-treated cells, 969 +/- 54 ng/10(5) cells; control cells, 370 +/- 15 ng/10(5) cells; LPS + NG-R1-treated cells, 469 +/- 29 ng/10(5) cells; n = 6). The 2.5- and 3.4-fold (2.2- and 3.2-kb) increases in PAI-1 mRNA levels induced by LPS (1 microgram/mL for 6 hours) were reduced to 1.4- and 2.6-fold increases in the presence of both LPS and 100 micrograms/mL NG-R1. LPS-induced tissue factor (TF) activity in HUVECs was also counteracted when the cells were coincubated with both LPS and 100 micrograms/mL NG-R1 for 6 hours (TF activity: LPS-treated cells, 88.6 +/- 6.5 mU/10(6) cells; control cells, 0.7 +/- 0.01 mU/10(6) cells; LPS + NG-R1-treated cells, 56.0 +/- 1.9 mU/10(6) cells). The 26-fold increase in TF mRNA levels induced by LPS (1 microgram/mL for 2 hours) was reduced to a 13-fold increase in the presence of both LPS and 100 micrograms/mL NG-R1. PAI activity levels in the plasma of mice 4 hours after injection of LPS (10 ng/g body wt) increased 2.3-fold compared with a control group. In contrast, PAI activity from LPS + NG-R1 (1 microgram/g body wt NG-R1)-treated animals was at control level (PAI-1 activity: LPS-treated group, 11.3 +/- 3.1 U/mL; control group, 4.9 +/- 0.3 U/mL; LPS + NG-R1-treated group, 4.3 +/- 1.0 U/mL; n = 5 to 8). The production of TNF-alpha induced by 1 microgram/mL LPS by cultured human whole-blood cells was inhibited by 46% when the cells were incubated together with 100 micrograms/mL NG-R1. NG-R1 protected mice from the lethal effects of LPS. The 78% lethality induced by LPS/galactosamine was reduced to 23% when NG-R1 was administered simultaneously (P < .01 by chi 2 test). To extend this study to inflammatory cells, the effect of NG-R1 on LPS stimulation of the monocytic cell line THP-1 was investigated. NG-R1 inhibited the LPS-induced degradation of I kappa B-alpha and superinduced LPS-induced I kappa B-alpha mRNA, indicating that the effect of NG-R1 is not restricted to endothelial cells and is at least in part mediated by interference with the NF-kappa B/I kappa B-alpha pathway.

Animals↗