How does LPS cause cell death?
Neuronal tissue in cortex and hippocampus are particularly susceptible. In this study, we report that LPS induces cell death as measured by caspase-3 activation and DNA fragmentation and that this is coupled with stimulation of the mitogen-activated protein kinase, p38.
What does LPS do to mice?
High concentrations of LPS leads to a septic shock, characterized by hypotension and multiple organ failures, and finally to death18. Mice are less sensitive to LPS compared to humans, where LPS concentrations between 2-4 ng/kg body weight (BW) are able to induce a cytokine storm19.
Does LPS cause necrosis?
As shown in Figure 5a, LPS induced robust necrosis in primary bone marrow-derived macrophages (BMDMs) in the presence of zVADfmk.
How does LPS cause cell damage?
Lipopolysaccharide (LPS) is a natural adjuvant synthesized by gram-negative bacteria that has profound effects on CD4 T cell responses. LPS stimulates cells through Toll-like receptor 4 (TLR4), causing the release of inflammatory cytokines and upregulation of costimulatory molecules on antigen presenting cells.
Is LPS a neurotoxin?
Our results indicate that the neurotoxic effects of LPS on nigral dopaminergic neurons are mediated by microglial activation, interleukin-1beta, and caspase-11 expression in mice.
What is LPS treatment?
LPS-treatment for 6 hours increased the expression levels of pro-inflammatory and chemotactic cytokines (TNF-a, IL-1ß, IL-6, CCL2, CCL5, IL-8), whereas 48 hour-treatment elevated the expression of anti-inflammatory factors (IL-10 and IL-6). LPS led to cell injury resulting from exaggerated cell apoptosis and necrosis.
Does LPS cause apoptosis?
LPS induces the autocrine secretion of TNF-, which produces apoptosis. (A) LPS induces the mRNA expression of TNF-α. Total RNA (20 μg per lane) from macrophages was treated with 100 ng/mL of LPS for the indicated times was analyzed by Northern blotting.
Why is LPS toxic?
The real, physical border that separates the inside of a bacterial cell from the outside world is its membrane, a double lipid layer interspersed with proteins, to which LPS is connected via lipid A, a phosphorylated lipid. The toxicity of LPS is mainly due to this lipid A, while the polysaccharides are less toxic.
Why is LPS a virulence factor?
The virulence factors of the lipopolysaccharide of Shigella species bacteria include the endotoxic activities of the lipid A component of the molecule and the ability of the polysaccharide chain--the core and the O-antigenic polysaccharide--to provide the bacterium with resistance to host defense mechanisms such as ...
What is LPS gut poisoning?
Leaky gut syndrome is a digestive condition that affects the lining of the intestines. In leaky gut syndrome, gaps in the intestinal walls allow bacteria and other toxins to pass into the bloodstream. Many doctors and healthcare professionals do not recognize leaky gut syndrome (LGS) as a diagnosable condition.
What are the roles of interleukin-6 in neonatal brain injury?
In the present study, the role (s) of interleukin-6 in mediating lipopolysaccharide-induced brain injury and behavioral changes was investigated by the intracerebral injection of lipopolysaccharide with interleukin-6 neutralizing antibody in the 5-day-old rat brain. Brain injury was examined in brain sections at postnatal day 8 and postnatal day 21. Behavioral tests including righting reflex, wire hanging maneuver, cliff avoidance, locomotor activity, gait analysis, responses in the elevated plus-maze and passive avoidance were performed from postnatal day 3 to postnatal day 21. Changes in astroglia, microglia and oligodendrocytes were studied using immunohistochemistry in the postnatal day 21 rat brain. Our results show that interleukin-6 antibody attenuated lipopolysaccharide-induced brain lateral ventricle dilation and improved neurobehavioral performance. Interleukin-6 antibody also suppressed lipopolysaccharide-induced astrogliosis and microglial activation, and increased the number of oligodendrocytes in white matter. However, no changes of tumor necrosis factor-α and interleukin-1β were detected. In contrast, no histopathological changes and glial activation were observed in rats injected with only interleukin-6. The present study indicates that the contribution to brain injury by interleukin-6 depends on its interaction with other lipopolysaccharide-induced agents and not on interleukin-6 alone.
How many arms are there in a plus maze?
The plus-maze consists of two open arms (30×5×0.25) and two enclosed arms (30×5×10 cm) emanating from a common central platform (5×5 cm) to form a plus shape. The entire apparatus was elevated to a height of 40 cm above the floor. A video camera and illuminating-lamps were mounted at the ceiling. The anxiety-related behaviors were recorded for a period of 5 min by a VCR-recording system on P19. The parameters recoded were the numbers of open or enclosed arm entries (arm entry defines as all four paws into an arm), and the time the animals spent in the various sections of the maze (open arm, center, enclosed arm) ( Sasaki et al., 2002 ).
Does IL-6 cause neurobehavioral deficits?
This study was undertaken to determine the role of IL-6 in mediating LPS-induced brain injury and neurobehavioral deficits. This is the first study to report that neutralizing the activity of the proinflammatory cytokine IL-6, using monoclonal IL-6 antibody, after LPS treatment, significantly attenuated brain injury, prevented the loss of OLs, suppressed activation of microglia and astrocytes, and improved most neurobehavioral performances. However, direct intracerebral application of IL-6 alone to the neonatal rat brain did not result in any apparent histopathological changes and glial activation. The results presented here indicate that IL-6 may play a deleterious role in LPS-induced brain damage as well as neurobehavioral deficits, while it was unable to induce visible brain injury or glial activation in the developing brain when given alone.
How did the plague affect society?
The plague profoundly altered society. Society buckled as people at all levels, from nobles to peasants, died in large numbers. Renters died and were not replaced, weakening the power of the landed gentry. Peasant revolts took place in England, France, Belgium and Italy. Entire villages were wiped out.
What is the name of the bacterium that infects mice and squirrels?
Scientists believe it was the bubonic plague, also known as the bacterium Yersinia pestis. Yersinia pestis typically infects the Oriental rat flea, which in turn infects small rodents such as mice, rodents and squirrels. As their rodent hosts die, infected fleas seek and bite humans.
What was the Black Death?
The Black Death was a tremendous tragedy for Europe, but it was also the impetus for societal upheaval. The Europe that emerged was traumatized but more dynamic than ever, set on a slow path of philosophical, scientific and geographic discovery that eventually spread worldwide.
Where did the plague come from?
From Italy the plague swept across Europe, replicating the tragedy of Genoa over and over again. The plague crossed the continent in waves and from multiple points of entry, not just Genoa, but typically through trading routes. By August 1348, it had reached southern England, and by 1350 had breached Scandinavia. By 1353, it had reached Moscow.
When was the first plague in Europe?
The first appearance of the plague in Europe was at Genoa in October 1347. One hypothesis is that Italian traders caught the plague during the Mongol siege of the Crimean city of Caffa, where the attackers allegedly hurled the bodies of plague victims over the city walls.
Where did the Black Death originate?
The disease that was later called the “Black Death” is thought to have originated on the steppes of Central Asia, gradually brought westward along trade routes. The first appearance of the plague in Europe was at Genoa in October 1347.
Was the plague a permanent disease?
Yet as widespread and deadly as it was, the plague never became a permanent resident of Europe. This and other factors, such as the unusual speed at which it spread and the lack of recorded rat die-offs, suggest to some scientists an Ebola-like hemorrhagic disease was actually responsible.
