Use of Meso-Scale Discovery™ to Examine Cytokine Content in Microglia Cell Supernatant

Burguillos, Miguel Ángel

doi:10.1007/978-1-62703-520-0_11

Cited by 18 publications

(10 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The levels of cytokines were measured using an electrochemi-luminescence-based multi-array method through the Quickplex SQ 120 system (Meso Scale Diagnostics LLC, Rockville, MD) by previously reported methods [ 46 – 49 ]. In brief, the system utilizes 96-well-based high throughput readout.…”

Section: Methodsmentioning

confidence: 99%

Cytokine-mediated inflammation mediates painful neuropathy from metabolic syndrome

et al. 2018

View full text Add to dashboard Cite

Painful neuropathy (PN) is a prevalent condition in patients with metabolic syndrome (MetS). However, the pathogenic mechanisms of metabolic syndrome-associated painful neuropathy (MetSPN) remain unclear. In the current study, high-fat-fed mice (HF mice) were used to study MetSPN. HF mice developed MetS phenotypes, including increased body weight, elevated plasma cholesterol levels, and insulin resistance in comparison with control-fat-fed (CF) mice. Subsequently, HF mice developed mechanical allodynia and thermal hyperalgesia in hind paws after 8 wk of diet treatment. These pain behaviors coincided with increased densities of nociceptive epidermal nerve fibers and inflammatory cells such as Langerhans cells and macrophages in hind paw skin. To study the effect of MetS on profiles of cytokine expression in HF mice, we used a multiplex cytokine assay to study the protein expression of 12 pro-inflammatory and anti-inflammatory cytokines in dorsal root ganglion and serum samples. This method detected the elevated levels of proinflammatory cytokines, including tumor necrosis factor (TNF)-α, and interleukin (IL)-6, IL-1β as well as reduced anti-inflammatory IL-10 in lumbar dorsal root ganglia (LDRG) of HF mice. Intraperitoneal administration of IL-10 reduced the upregulation of pro-inflammatory cytokines and alleviated pain behaviors in HF mice without affecting MetS phenotypes. Our findings suggested targeting HF-induced cytokine dysregulation could be an effective strategy for treating MetSPN.

show abstract

Section: Methodsmentioning

confidence: 99%

Cytokine-mediated inflammation mediates painful neuropathy from metabolic syndrome

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Compared with the traditional ELISA approach, the MSD platform shows greater sensitivity and is able to reliably detect different proteins across a broad dynamic range of concentrations [20]. The assay is based upon electro-chemiluminescence technology by using specific capture antibodies coated at corresponding spots on an electric wired microplate.…”

Section: Methodsmentioning

confidence: 99%

Serum thyroid-stimulating hormone and interleukin-8 levels in boys with autism spectrum disorder

Singh

Yazdani

Gadad

et al. 2017

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundAutism spectrum disorder (ASD) affects approximately 1 in 68 children in the USA. An ASD blood biomarker may enable early diagnosis and/or identification of new therapeutic targets. Serum samples from ASD and typically developing (TD) boys (n = 30/group) were screened for differences in 110 proteins using a multiplex immunoassay.ResultsEleven proteins were found that together could confirm ASD with modest accuracy using multiple training and test sets. Two of the 11 proteins identified here were further tested using a different detection platform and with a larger sample of ASD and TD boys. The two proteins, thyroid-stimulating hormone (TSH) and interleukin-8 (IL-8), have been previously identified as putative biomarkers for ASD. TSH levels were significantly lower in ASD boys, whereas IL-8 levels were significantly elevated. The diagnostic accuracy for ASD based upon TSH or IL-8 levels alone varied from 74 to 76%, but using both proteins together, the diagnostic accuracy increased to 82%. In addition, TSH levels were negatively correlated with the Autism Diagnostic Observation Schedule subdomain scores.ConclusionsThese data suggest that a panel of proteins may be useful as a putative blood biomarker for ASD.

show abstract

“…Cytokine proteins in plasma and hippocampal homogenates were quantified using a customized Meso-Scale Discovery (MSD) V-Plex electrochemiluminescence assay for mice, which allows ultralow detection of multiple cytokines in mouse plasma and supernatants [ 44 ]. V-plex plus 96-well plates coated with primary antibodies directed against interleukin (IL)-1β, IL-4, IL-6, and tumor necrosis factor (TNF)-α were used and were treated with the corresponding detecting antibodies, which were prelabeled with SULFO-TAG™ (MSD, Rockville, Maryland, USA).…”

Section: Methodsmentioning

confidence: 99%

Late prenatal immune activation causes hippocampal deficits in the absence of persistent inflammation across aging

Giovanoli

Notter

Richetto

et al. 2015

J Neuroinflammation

View full text Add to dashboard Cite

BackgroundPrenatal exposure to infection and/or inflammation is increasingly recognized to play an important role in neurodevelopmental brain disorders. It has recently been postulated that prenatal immune activation, especially when occurring during late gestational stages, may also induce pathological brain aging via sustained effects on systemic and central inflammation. Here, we tested this hypothesis using an established mouse model of exposure to viral-like immune activation in late pregnancy.MethodsPregnant C57BL6/J mice on gestation day 17 were treated with the viral mimetic polyriboinosinic-polyribocytidilic acid (poly(I:C)) or control vehicle solution. The resulting offspring were first tested using cognitive and behavioral paradigms known to be sensitive to hippocampal damage, after which they were assigned to quantitative analyses of inflammatory cytokines, microglia density and morphology, astrocyte density, presynaptic markers, and neurotrophin expression in the hippocampus throughout aging (1, 5, and 22 months of age).ResultsMaternal poly(I:C) treatment led to a robust increase in inflammatory cytokine levels in late gestation but did not cause persistent systemic or hippocampal inflammation in the offspring. The late prenatal manipulation also failed to cause long-term changes in microglia density, morphology, or activation, and did not induce signs of astrogliosis in pubescent, adult, or aged offspring. Despite the lack of persistent inflammatory or glial anomalies, offspring of poly(I:C)-exposed mothers showed marked and partly age-dependent deficits in hippocampus-regulated cognitive functions as well as impaired hippocampal synaptophysin and brain-derived neurotrophic factor (BDNF) expression.ConclusionsLate prenatal exposure to viral-like immune activation in mice causes hippocampus-related cognitive and synaptic deficits in the absence of chronic inflammation across aging. These findings do not support the hypothesis that this form of prenatal immune activation may induce pathological brain aging via sustained effects on systemic and central inflammation. We further conclude that poly(I:C)-based prenatal immune activation models are reliable in their effectiveness to induce (hippocampal) neuropathology across aging, but they appear unsuited for studying the role of chronic systemic or central inflammation in brain aging.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-015-0437-y) contains supplementary material, which is available to authorized users.

show abstract

Use of Meso-Scale Discovery™ to Examine Cytokine Content in Microglia Cell Supernatant

Cited by 18 publications

References 4 publications

Cytokine-mediated inflammation mediates painful neuropathy from metabolic syndrome

Cytokine-mediated inflammation mediates painful neuropathy from metabolic syndrome

Serum thyroid-stimulating hormone and interleukin-8 levels in boys with autism spectrum disorder

Late prenatal immune activation causes hippocampal deficits in the absence of persistent inflammation across aging

Contact Info

Product

Resources

About