scholarly journals Identification of the Cellular Sensor That Stimulates the Inflammatory Response to Sterile Cell Death

2010 ◽  
Vol 184 (8) ◽  
pp. 4470-4478 ◽  
Author(s):  
Hajime Kono ◽  
Dipti Karmarkar ◽  
Yoichiro Iwakura ◽  
Kenneth L. Rock
Keyword(s):  
Cell Death ◽  
Inflammatory Response ◽  
Sterile Cell

scholarly journals Uric acid promotes an acute inflammatory response to sterile cell death in mice

2010 ◽  
Vol 120 (6) ◽  
pp. 1939-1949 ◽  
Author(s):  
Hajime Kono ◽  
Chun-Jen Chen ◽  
Fernando Ontiveros ◽  
Kenneth L. Rock
Keyword(s):  
Cell Death ◽  
Uric Acid ◽  
Inflammatory Response ◽  
Acute Inflammatory Response ◽  
Sterile Cell

Methylisothiazolinone may induce cell death and inflammatory response through DNA damage in human liver epithelium cells

2017 ◽  
Vol 33 (2) ◽  
pp. 156-166 ◽  
Author(s):  
Eun-Jung Park ◽  
Sanghwa Kim ◽  
Jaerak Chang
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Inflammatory Response ◽  
Human Liver ◽  
Induce Cell Death ◽  
Epithelium Cells

scholarly journals TNFα-induced AMPA-receptor trafficking in CNS neurons; relevance to excitotoxicity?

2004 ◽  
Vol 1 (3) ◽  
pp. 263-273 ◽  
Author(s):  
DMITRI LEONOUDAKIS ◽  
STEVEN P. BRAITHWAITE ◽  
MICHAEL S. BEATTIE ◽  
ERIC C. BEATTIE
Keyword(s):  
Cell Death ◽  
Inflammatory Response ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cell Types ◽  
Synaptic Function ◽  
Ampar Trafficking ◽  
Novel Target

Injury and disease in the CNS increases the amount of tumor necrosis factor α (TNFα) that neurons are exposed to. This cytokine is central to the inflammatory response that occurs after injury and during prolonged CNS disease, and contributes to the process of neuronal cell death. Previous studies have addressed how long-term apoptotic-signaling pathways that are initiated by TNFα might influence these processes, but the effects of inflammation on neurons and synaptic function in the timescale of minutes after exposure are largely unexplored. Our published studies examining the effect of TNFα on trafficking of AMPA-type glutamate receptors (AMPARs) in hippocampal neurons demonstrate that glial-derived TNFα causes a rapid (<15 minute) increase in the number of neuronal, surface-localized, synaptic AMPARs leading to an increase in synaptic strength. This indicates that TNFα-signal transduction acts to facilitate increased surface localization of AMPARs from internal postsynaptic stores. Importantly, an excess of surface localized AMPARs might predispose the neuron to glutamate-mediated excitotoxicity and excessive intracellular calcium concentrations, leading to cell death. This suggests a new mechanism for excitotoxic TNFα-induced neuronal death that is initiated minutes after neurons are exposed to the products of the inflammatory response.Here we review the importance of AMPAR trafficking in normal neuronal function and how abnormalities that are mediated by glial-derived cytokines such as TNFα can be central in causing neuronal disorders. We have further investigated the effects of TNFα on different neuronal cell types and present new data from cortical and hippocampal neurons in culture. Finally, we have expanded our investigation of the temporal profile of the action of this cytokine relevant to neuronal damage. We conclude that TNFα-mediated effects on AMPAR trafficking are common in diverse neuronal cell types and very rapid in their onset. The abnormal AMPAR trafficking elicited by TNFα might present a novel target to aid the development of new neuroprotective drugs.

PPE11 of Mycobacterium tuberculosis can alter host inflammatory response and trigger cell death

2019 ◽  
Vol 126 ◽  
pp. 45-55 ◽  
Author(s):  
Xuan Peng ◽  
Tao Luo ◽  
Xiaoqian Zhai ◽  
Chunxi Zhang ◽  
Jing Suo ◽  
...  
Keyword(s):  
Cell Death ◽  
Mycobacterium Tuberculosis ◽  
Inflammatory Response ◽  
Trigger Cell Death ◽  
Host Inflammatory Response

scholarly journals Inflammatory Response Elicited by Ureaplasma parvum colonization in human cervical epithelial, stromal, and immune cells

Reproduction ◽  
2021 ◽  
Author(s):  
Ourlad Alzeus Gaddi Tantengco ◽  
Talar Kechichian ◽  
Kathleen L Vincent ◽  
Richard B Pyles ◽  
Paul Mark B Medina ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Stromal Cells ◽  
Female Reproductive Tract ◽  
Ureaplasma Parvum ◽  
Cervical Epithelial Cells ◽  
Anti Inflammatory ◽  
The Impact

Ureaplasma parvum is a commensal bacterium in the female reproductive tract but has been associated with pregnancy complications such as preterm prelabor rupture of membranes and preterm birth (PTB). However, the pathologic effects of U. parvum in the cervix, that prevents ascending infections during pregnancy, are still poorly understood. To determine the impact of U. parvum on the cervix, ectocervical (ecto) and endocervical (endo) epithelial and stromal cells were incubated with U. parvum. Macrophages were also tested as a proxy for cervical macrophages to determine the antigenicity of U. parvum. The effects of U. parvum, including influence on cell cycle and cell death, antimicrobial peptide production, epithelial-to-mesenchymal transition (EMT), and inflammatory cytokine levels, were assessed. U. parvum colonized cervical epithelial and stromal cells 4 hours post-infection. Like uninfected control, U. parvum neither inhibited cell cycle progression and nor caused cell death in cervical epithelial and stromal cells. U. parvum increased the production of the antimicrobial peptides (AMPs) cathelicidin and human β-defensin 3 and exhibited weak signs of EMT evidenced by decreased cytokeratin 18 and increased vimentin expression in cervical epithelial cells. U. parvum induced a pro-inflammatory environment (cytokines) and increased MMP-9 in cervical epithelial cells but promoted pro- and anti-inflammatory responses in cervical stromal cells and macrophages. U. parvum may colonize the cervical epithelial layer, but induction of AMPs and anti-inflammatory response may protect the cervix and may prevent ascending infections that can cause PTB. These findings suggest that U. parvum is a weak inducer of inflammation in the cervix.

Continuous subcutaneous infusion of pramipexole protects against lipopolysaccharide-induced dopaminergic cell death without affecting the inflammatory response

2008 ◽  
Vol 212 (2) ◽  
pp. 522-531 ◽  
Author(s):  
Mahmoud M. Iravani ◽  
Mona Sadeghian ◽  
Clement C.M. Leung ◽  
Banu C. Tel ◽  
Sarah Rose ◽  
...  
Keyword(s):  
Cell Death ◽  
Inflammatory Response ◽  
Dopaminergic Cell ◽  
Subcutaneous Infusion ◽  
Continuous Subcutaneous Infusion

scholarly journals Minocycline reduces inflammatory response and cell death in a S100B retina degeneration model

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Pia Grotegut ◽  
Natarajan Perumal ◽  
Sandra Kuehn ◽  
Andreas Smit ◽  
H. Burkhard Dick ◽  
...  
Keyword(s):  
Cell Death ◽  
Body Weight ◽  
Optic Nerve ◽  
Inflammatory Response ◽  
Negative Impact ◽  
Dependent Manner ◽  
Label Free ◽  
Proteomics Analysis ◽  
Concentration Dependent Manner ◽  
Minocycline Treatment

Abstract Background Previous studies noted that intravitreal injection of S100B triggered a glaucoma-like degeneration of retina and optic nerve as well as microglia activation after 14 days. The precise role of microglia in our intravitreal S100B model is still unclear. Hence, microglia were inhibited through minocycline. The aim is to investigate whether microglia have a significant influence on the degeneration process or whether they are only a side effect in the model studied here. Methods Minocycline was applied daily in rats by intraperitoneal injection using two different concentrations (13.5 mg/kg body weight, 25 mg/kg body weight). One day after treatment start, S100B or PBS was intravitreally injected in one eye per rat. The naïve groups received no injections. This resulted in a total of five groups (naïve n = 14, PBS n = 14, S100B n = 13, 13.5 mg/kg mino n = 15, 25 mg/kg mino n = 15). At day 14, electroretinogram measurements were performed, followed by immunofluorescence and label-free quantitative proteomics analysis. The focus of these investigations was on the survival of RGCs as well as their axons, the response of the microglia, and the identification of further pathological modes of action of S100B. Results The best signal transmission was detected via ERG in the 13.5 mg/kg mino group. The inhibition of the microglia protected optic nerve neurofilaments and decreased the negative impact of S100B on RGCs. However, the minocycline treatment could not trigger complete protection of RGCs. Furthermore, in retina and optic nerve, the minocycline treatment reduced the number and activity of S100B-triggered microglia in a concentration-dependent manner. Proteomics analysis showed that S100B application led to numerous metabolic functions and cellular stress, mainly an increased inflammatory response, glycolysis, and mitochondrial dysfunction, which caused oxidative stress in the retina. Importantly, the protective capability of lower dose of minocycline was unraveled by suppressing the apoptotic, inflammatory, and the altered metabolic processes caused by S100B insult in the retina. Conclusion Intravitreally injected S100B not only led to a pro-inflammatory microglial reaction, but also a mitochondrial and metabolic dysfunction. Also, these results suggest that an excessive microglial response may be a significant degenerative factor, but not the only trigger for increased cell death.

scholarly journals Enrichment of ATP Binding Proteins Unveils Proteomic Alterations in Human Macrophage Cell Death, Inflammatory Response, and Protein Synthesis after Interaction with Candida albicans

2019 ◽  
Vol 18 (5) ◽  
pp. 2139-2159 ◽  
Author(s):  
Catarina Vaz ◽  
Jose Antonio Reales-Calderon ◽  
Aida Pitarch ◽  
Perceval Vellosillo ◽  
Marco Trevisan ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Synthesis ◽  
Candida Albicans ◽  
Inflammatory Response ◽  
Binding Proteins ◽  
Human Macrophage ◽  
Atp Binding ◽  
Macrophage Cell
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