scispace - formally typeset
Search or ask a question

What are the effect of LPS infusions in terms of effect in microglia, astrocyte and cytokines? 


Best insight from top research papers

Lipopolysaccharide (LPS) infusions induce significant effects on microglia, astrocytes, and cytokines. LPS administration triggers microglial activation and alters their morphology, leading to synaptic dysfunction and cognitive impairment over a defined temporal sequence . Additionally, LPS exposure results in the activation of glial-specific genes, particularly in microglia, and induces differential alternative splicing in astrocytes, affecting immune-specific responses . Furthermore, LPS injections lead to peripheral and central increases in pro-inflammatory cytokines, impacting microglia activation in a strain and sex-dependent manner . Overall, LPS infusion disrupts the neurovascular unit by affecting the interactions between perivascular astrocytes and microglia, contributing to neuroinflammation and potential blood-brain barrier integrity loss .

Answers from top 5 papers

More filters
Papers (5)Insight
LPS infusions activate microglia, increase inflammatory cytokines (IL-6, TNF-α), and decrease dopaminergic neurons, contributing to depression in a Parkinson's disease-like condition. Astrocytes were not specifically mentioned.
LPS infusions induce strain and sex-dependent changes in microglia activation, astrocyte percentage, and cytokine levels, particularly TNF-α, IL-1β, and IL-6 in male mice.
LPS infusions induce microglial activation, GABAergic synaptic deficits, and prolonged cognitive impairment, but the effects on astrocytes and cytokines are not specifically addressed in the paper.
LPS infusion triggers microglial and astrocytic activation, altering their interactions with vasculature, potentially compromising BBB integrity. Cytokines like IL-1a, TNFa, and C1q play key roles in this process.
LPS infusions impact microglia and astrocytes, with Ptbp1 exon 8 skipping modulating immune response. Alternative splicing affects immune-related genes, suggesting a role in brain immune modulation.

Related Questions

How does intraperitoneal LPS administration affect the composition and function of intestinal mucus?5 answersIntraperitoneal administration of lipopolysaccharides (LPS) can significantly impact the composition and function of intestinal mucus. Studies have shown that exposure to LPS can lead to changes in the mucus layer thickness and goblet cell functions in the small intestine. Low doses of LPS can increase mucus layer thickness and enhance the barrier function of the intestine against luminal bacteria, while high doses of LPS can result in a decrease in mucus layer thickness, compromising the intestinal mucosal barrier and leading to chronic low-grade inflammation. Additionally, the expression of mucin-2 (MUC2), a major component of the mucus layers, is significantly increased in response to LPS exposure, especially in the uterus, suggesting a protective role of MUC2 against LPS translocation into uterine tissue.
What is the impact of LPS and butyrate on cytokine release in Caco2 cells?4 answersButyrate has been shown to have an impact on cytokine release in Caco2 cells. It has been found to modulate inflammatory cytokine release by activated peripheral blood mononuclear cells (PBMCs) in a co-culture model with Caco2 cells, leading to a decrease in the release of interleukin-1 beta, tumor necrosis factor alpha, interleukin-17a, interferon gamma, and interleukin-10. Additionally, butyrate treatment induced the secretion of tumor necrosis factor-alpha in SW480 and CT26 cells. Furthermore, butyrate was found to attenuate the upregulation of claudin-2 induced by tumor necrosis factor-alpha and interferon-gamma in Caco2 cells. These findings suggest that butyrate can modulate cytokine release in Caco2 cells, potentially influencing inflammatory processes in the intestine.
What are the effects of lipopolysaccharide on microglia?4 answersLipopolysaccharide (LPS) has various effects on microglia. LPS treatment increases microglial GABA uptake and GABA transporter (GAT)-1 trafficking, which can trigger the inflammatory response by altering microglial GABA clearance. LPS-induced microglial activation is accompanied by the induction of CD147 expression, and inhibiting CD147 expression can inhibit LPS-induced microglial inflammatory activation. LPS treatment also leads to microglia activation and neuroinflammation, but D-beta-hydroxybutyrate (BHB) treatment attenuates these effects by reducing the generation of inflammatory cytokines and promoting the generation of protective factors. LPS-induced neuroinflammation can be attenuated by triggering the receptor expressed on myeloid cells 2 (TREM2), which modulates microglial polarization from M1 to M2 phenotype. LPS stimulation of iPSC-microglia induces a transcriptional response, and LPS+IFN-γ stimulation shows a convergent mechanism of action with ATPγS stimulation.
What is the mean lethal dose of LPS in rats?5 answersThe mean lethal dose of LPS in rats is 10 mg in male Sprague Dawley (SD) rats. Female rats may be more resistant to LPS-induced sepsis. In pregnant Wistar rats, a dose of 150 μg/kg of LPS caused death in 23.07% of the rats. In another study, LPS at a concentration of 3 mg/kg caused death after 95 minutes in rats. The survival time was increased to 190 minutes with pretreatment of Bronco T (BT) or pentoxifylline (PTX). The PTX showed a better response with a survival rate of 75% compared to BT with a survival rate of 72%.
How does LPS administration affect the brain mice?3 answersLPS administration in mice induces neuroinflammation and affects brain function. Studies have shown that LPS injection leads to the activation of inflammation and subsequent depression-like behavior in mice. Mild neuroinflammation induced by LPS also results in region-specific microglial activation and the production of pro-inflammatory cytokines in different brain regions. Additionally, LPS exposure has been found to impair the glymphatic system, which is responsible for waste clearance in the brain, leading to decreased perivascular distribution of cerebrospinal fluid (CSF). Prenatal exposure to LPS has also been shown to have long-lasting effects on offspring, including increased inflammation, altered cortical cytoarchitecture, and behavioral impairments. Overall, LPS administration in mice has been found to have significant effects on neuroinflammation, microglial activation, glymphatic function, and brain development and behavior.
Does lps induce inflammatory response in macrophage cell lines and human colon cancer cells?5 answersLPS induces an inflammatory response in macrophage cell lines and human colon cancer cells. Bacterial LPS activates cells of the macrophage/monocyte lineage, leading to the release of arachidonic acid and activation of cytosolic PLA2 in macrophage cell lines. LPS also causes iNOS synthesis and formation of free radicals in microglia and macrophages, contributing to post-traumatic inflammation. Additionally, LPS stimulates cytokine synthesis and release in macrophages, as well as macrophage migration. Furthermore, LPS-mediated production and secretion of cytokines and chemokines are decreased by an ethanolic extract of Artocarpus lakoocha Roxb. in macrophage cell lines. Therefore, LPS induces an inflammatory response in macrophage cell lines and human colon cancer cells, leading to the release of inflammatory mediators and activation of various signaling pathways.

See what other people are reading

How HDL affects cognitive function?
5 answers
High-density lipoprotein cholesterol (HDL) plays a crucial role in cognitive function among older adults. Research indicates that higher levels of HDL are associated with better cognitive performance. Longitudinal studies suggest that an increase in non-high-density lipoprotein cholesterol (NHDL-C) may be protective against cognitive decline, particularly in females and individuals without cardiovascular disease. Furthermore, a higher concentration of total cholesterol, including HDL, is linked to improved cognitive scores in elderly females without a history of stroke. HDL's protective effects on cognitive function are attributed to its ability to reduce amyloid β-protein accumulation, vascular inflammation, and neuroinflammation, ultimately preserving memory function in the elderly. In summary, maintaining high levels of HDL may serve as a protective factor against cognitive impairment in aging individuals.
What are preventive measures for Alzheimer's disease?
5 answers
Preventive measures for Alzheimer's disease include lifestyle interventions such as education, social engagement, cognitive stimulation, exercise, and maintaining a healthy diet. Additionally, dietary components like soy isoflavones, rutin, and vitamin B1 have shown neuroprotective effects against AD. Modifiable risk factors like substance use, lack of physical and mental activity, and poor sleep habits should be addressed to delay the onset of AD. Screening tools like biomarkers and cognitive assessments are crucial for early detection and effective care planning. Primary prevention strategies targeting healthy seniors through non-pharmacological treatments like physical exercise and a healthy diet can help prevent the progression of AD. Overall, a combination of these approaches can significantly reduce the risk of developing Alzheimer's disease.
What are the research gaps in the field of altitude hypoxia causing breast cancer?
5 answers
Research on altitude hypoxia causing breast cancer has identified several gaps. Firstly, the impact of hypoxia on DNA repair pathways and mutational burden in breast cancer cells remains incompletely understood. Secondly, the volatilomic response to hypoxia in aggressive vs. non-aggressive breast cancer cells needs further exploration. Additionally, the metabolic reprogramming induced by hypoxia in breast tumor-repopulating cells (TRCs) and its role in promoting tumor growth requires more investigation. Furthermore, the mechanism by which hypoxia alters DNA methylation through TET1/3 enzymes to drive breast tumor-initiating cell (BTIC) properties is a crucial area for future research. Lastly, the impact of hypoxia on alternative splicing events in breast cancer cells and their implications in oncogenesis need more detailed study.
How the immune system might be involved in depression, including cytokine effects on neurons and neurotransmitters?
5 answers
The immune system plays a crucial role in depression, with evidence pointing towards immune activation contributing to the pathogenesis of the disorder. Studies have shown that immune activation, characterized by increased pro-inflammatory cytokines, is associated with depression. In particular, cytokines like interleukin-1β, interleukin-6, and tumor necrosis factor-α have been implicated in depression, affecting neuronal function and neurotransmitter activity. Additionally, alterations in T cell subtypes, especially Th17 cells producing interleukin-17A, have been linked to depression, influencing the gut-brain axis and stress responses. These findings suggest that immune-mediated mechanisms, including cytokine effects on neurons and neurotransmitters, play a significant role in the pathophysiology of depression, opening avenues for immune-modulating treatments in depression therapy.
What elements of postpartum depression does allopregnanolone treatment effect?
5 answers
Allopregnanolone treatment impacts various elements of postpartum depression (PPD). Studies suggest that Allopregnanolone activates unique molecular pathways in women with PPD, potentially tied to its antidepressant mechanism. Allopregnanolone, a neurosteroid, positively modulates GABAA receptors, which are implicated in major depressive disorder, and its analog, brexanolone, has shown efficacy in improving depression scores in PPD trials. The FDA-approved brexanolone, a synthetic formulation of Allopregnanolone, offers rapid and effective treatment for PPD, enhancing the inhibitory effects of GABAA and mimicking a naturally produced progesterone metabolite crucial during pregnancy and postpartum. Allopregnanolone's effects on GABAergic inhibition, particularly at receptors containing the δ subunit, play a significant role in treating PPD.
What are the specific cell signaling pathways regulated by c-Abl kinase activation in response to Aβ fibrils?
5 answers
Activation of c-Abl kinase in response to Aβ fibrils leads to the regulation of specific cell signaling pathways. Studies have shown that c-Abl activation by AβOs induces synaptic damage and loss, with EphA4 being identified as an upstream regulator of c-Abl activation. Furthermore, c-Abl is known to play a crucial role in neurodegenerative diseases, including Alzheimer's disease, through mechanisms such as neuroinflammation, oxidative stress, and Tau protein phosphorylation. Additionally, c-Abl has been implicated in promoting myogenesis by activating the p38 α/β MAPK pathway in satellite cells, thereby influencing muscle regeneration. These findings collectively suggest that c-Abl kinase activation in response to Aβ fibrils impacts synaptic plasticity, neuroinflammation, and muscle regeneration through various signaling pathways.
How does the consumption of fruits impact the progression of Alzheimer's disease, according to research?
5 answers
Consumption of fruits can have varying impacts on the progression of Alzheimer's disease (AD) according to research. While fresh fruit intake did not show a significant causal relationship with AD risk, certain dietary phytochemicals, particularly polyphenols found in fruits, have demonstrated potential in modulating key AD pathologies like reducing β-amyloid plaques and neurofibrillary tangles. Additionally, nutritional deficiencies, including those related to fruit intake, are common in AD patients and may influence disease progression. Moreover, specific fruit components, like those found in miracle fruit seeds, have shown therapeutic implications in AD by affecting pathways related to insulin signaling and neurodegeneration. These findings highlight the complex relationship between fruit consumption and AD progression, suggesting both potential benefits and risks that warrant further investigation.
Do plasmalogen content in tissues decline with age?
5 answers
Plasmalogen content in tissues does decline with age, as supported by various research studies. Studies have shown that plasma choline plasmalogen levels decrease with age, particularly in relation to factors of atherosclerosis. Additionally, in aged female mice, supplementation with plasmalogens led to improved cognitive performance, synaptic plasticity, and neurogenesis, indicating a potential intervention strategy for halting neurodegeneration and promoting neuroregeneration. Furthermore, the reduction of plasmalogens has been associated with age-related neurodegenerative diseases like Alzheimer's disease, emphasizing the importance of these lipid species in maintaining neural health. Overall, the data from these studies collectively suggest a decline in plasmalogen content in tissues with age, highlighting the significance of these molecules in aging and age-related diseases.
What are Models of Trauma Transmission?
5 answers
Models of trauma transmission encompass various theoretical frameworks that explain the intergenerational transfer of trauma-related experiences. These models delve into the mechanisms through which trauma can be passed from one generation to the next, impacting parent-child relationships and attachment dynamics. The dissociative mechanism proposed by Main and Hesse, along with Lyons Ruth's model of emotional communication breakdown, are prominent theories in understanding the transmission of disorganized attachment from parents to children. Additionally, the exploration of trauma transmission within specific contexts, such as post-genocide Rwanda, sheds light on the determinants and pathways of PTSD transmission, emphasizing the complex interplay between parental trauma, attachment, and child traumatization.
What is the process of. the neuroimmunesystem starting fromo. how a pathogen enters ?
5 answers
The process of the neuroimmune system starts with the entry of a pathogen into the body. Pathogens trigger the production of cytokines like IL-1, TNFα, IL-6, and IFNγ, which act on peripheral neurons and vagus nerve terminals, transmitting signals to CNS neurons. The immune system, comprising innate and adaptive immunity, responds to the pathogen invasion. Innate immunity, with rapid non-specific responses, involves physical agents, cytokines, chemokines, and inflammatory cells, while adaptive immunity, specific and involving antibodies and antigen-specific T and B lymphocytes, works in tandem with innate responses to combat pathogens. In cases like neuroinflammatory diseases, the immune and nervous systems interact bidirectionally, impacting each other's functions under both normal and pathological conditions. Activated T cells exposed to antigens can cross the blood-brain barrier and migrate into the brain, paving the way for potential immunotherapy for central nervous system lesions.
How does chronic stress affect the glutamatergic transmission in the hippocampus?
5 answers
Chronic stress impacts glutamatergic transmission in the hippocampus through various mechanisms. Studies show that chronic stress can lead to alterations in ionotropic glutamate receptors, such as NMDA receptors, both at synaptic and extrasynaptic levels. Additionally, chronic stress can result in the dysregulation of metabotropic glutamate receptors (mGluRs) and Homer1 expression, affecting synaptic plasticity and depressive-like behaviors. Furthermore, chronic stress-induced downregulation of mGlu2 receptors may contribute to stress-related neuropsychiatric disorders by enhancing glutamate overflow in the hippocampus. These findings highlight the intricate ways in which chronic stress disrupts glutamatergic signaling in the hippocampus, potentially contributing to the pathophysiology of stress-related mood disorders.