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1,422 results for “Cytokines”
Cytokine storms and pyroptosis are primarily responsible for the rapid death of mice infected with pseudorabies virus
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Plasma cytokine measurements using Luminex in COVID-19 patients
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Inhibition of Cdc42 activity extends lifespan and decreases circulating inflammatory cytokines in aged female C57BL/6 mice
<p>Cdc42 is a small RhoGTPase regulating multiple functions in eukaryotic cells. The activity of Cdc42 is significantly elevated in several tissues of aged mice, while the Cdc42 gain-of-activity mouse model presents with a pre-mature aging-like phenotype and with decreased lifespan. These data suggest a causal connection between elevated activity of Cdc42, aging and reduced lifespan. Here, we demonstrate that systemic treatment of aged (75-week old) female C57BL/6 mice with a Cdc42 activity specific inhibitor (CASIN) for 4 consecutive days significantly extends average and maximum lifespan. Moreover, aged CASIN-treated animals displayed a youthful level of the aging-associated cytokines IL-1b, IL-1a and INFg in serum and a significantly younger epigenetic clock as based on DNA methylation levels in blood cells. Overall, our data show that systemic administration of CASIN to reduce Cdc42 activity in aged mice extends murine lifespan.</p>
Cytokine Data MIA Model
<p>The data set includes maternal and fetal cytokines, as measured by Meso Scale Discovery Electrochemiluminescence (<i>MSD</i>) in a poly(I:C)-based mouse model of maternal immune activation.</p>
CCL20 expression in human keratinocytes upon cytokine, pro-inflammatory, and UV stimuli.
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Effects of cold or warm ischemia and ex-vivo lung perfusion on the release of damage associated molecular patterns and inflammatory cytokines in experimental lung transplantation
<p>Lung transplantation (LTx) is associated with sterile inflammation, possibly related to the release of damage associated molecular patterns (DAMPs) by injured allograft cells. We have measured cellular damage and the release of DAMPs and cytokines in an experimental model of LTx after cold or warm ischemia and examined the effect of pretreatment with ex-vivo lung perfusion (EVLP).</p>
Resident self-tissue of proinflammatory cytokines rather than their systemic levels correlates with development of myelofibrosis in Gata1low mice
<p><strong>Movie 1</strong>: tridimensional image of GFP localization in the nucleus</p> <p><strong>Movie 2</strong>: tridimensional image of GFP localization in the cytoplasm</p> <p><strong>Movie 3</strong>: tridimensional reconstruction of GFPpositive cells localized around an adipocyte </p>
Resident self-tissue of proinflammatory cytokines rather than their systemic levels correlates with development of myelofibrosis in Gata1low mice
<p><strong>Figure S1. Gating used to identify endothelial cells (ECs), mesenchymal cells (MSCs), osteoblasts (OBCs), megakaryocytes (MKs) and neutrophils (Neu) in the bone marrow from a wild type mouse. </strong>In order to correctly estimate the frequency of all the cell populations, the monocellular cell suspension used for the analyses were prepared by carefully crushing the femurs of the mice (see [34] and [35] for detail).</p> <p><strong> Figure S2. (A) Example of the computer assisted image analysis used to quantify the level of fibrosis in bone marrow sections stained by Reticulin (black fibers) from representative wild-type (WT) and <em>Gata1</em><sup>low</sup> mice.</strong> The ImageJ program-assisted quantification process includes selection of the color channel (black histogram, Hue), determination of the threshold (Saturation histogram) and quantification of the areas which exceed the threshold (in %) (Brightness histogram). <strong>(B) Example of the computer assisted image analysis used to quantify the number of megakaryocytes positive per CXCR1 in in bone marrow sections from wild-type (WT) and <em>Gata1</em><sup>low</sup> mice. </strong>In this case, the conditions to quantify the signal in wild-type and <em>Gata1</em><sup>low</sup> mice were set separately. The ImageJ program-assisted quantification process includes selection of the cell type, determination of the threshold per cell (Saturation histogram) and quantification of the number of cells which exceed the threshold (Brightness histogram). Magnification 40x.</p> <p><strong>Figure S3. Levels of the proinflammatory cytokines </strong><strong>TGF-</strong><strong>β</strong><strong>1 (A), LCN2 (B) and CXCL1 (C) detected in the sera from wild-type, </strong><strong><em>Psel</em></strong><strong><sup>null</sup></strong><strong> and <em>Gata1</em><sup>low</sup><em>Psel</em><sup>null</sup> mice (all in the CD1 background).</strong> The levels of TGF-β1 in <em>Gata1</em><sup>low</sup> mice were previously reported [33] and are presented as median values from 20 mice as horizontal green line for comparison. Values are presented divided by gender (M, males; F, females) and age (adult and old). P values were calculated with Turkey’s multiple comparison test and are summarized either on the right or in <strong>Table S1</strong>. The number of mice analyzed in each experimental group is indicated by n.</p> <p><strong> Figure S4.<strong> </strong>Serum levels of pro-inflammatory cytokines (TGF-</strong><strong>β</strong><strong>1, upper panel; LCN2, middle panel; CXCL1, bottom panel) detected in CD1, C57BL/6 and DBA/2 mice</strong>. Gender (M, males; F, females) and age (adult and old) were analyzed as independent variables. The number of mice analyzed in each experimental group is indicated by n. Significant p values calculated with multiple comparison performed separately among groups from each different genotype are indicated in the graph. P values obtained with Turkey’s multiple comparison test among all groups are summarized in supplementary <strong>Tables S2-S4</strong>.</p> <p><strong> Figure S5. Hematoxylin/Eosin (H&E) and reticulin staining and TGF-β1, LCN2 and CXCL1 immunostaining of bone marrow sections from representative wild-type (WT) and <em>Gata1</em><sup>low</sup> littermates showing the fibrosis and increased cytokine bioavailability in the microenvironment of the mutant mice. </strong>Results are representative of those observed in 12-month old mice randomly selected from male and female, at least were analyzed 6 mice each staining. The arrows indicate individual megakaryocytes in wild-type mice and megakaryocyte clusters in <em>Gata1</em><sup>low</sup> mice. Magnification 40x. Similar results were previously published in Dunbar et al, 2021[11].</p> <p><strong>Figure S6</strong><em>. </em><strong>Immunohistochemical staining with (P+S) and without (S) the primary antibodies of consecutive sections from the bone marrow of WT and </strong><em>Gata1</em><sup>low</sup><strong> mice showing the specificity of the staining with the primary antibodies. </strong></p> <p><strong>Figure S7. The bone marrow from <em>Gata1</em><sup>low</sup> mice contain great levels of CXCR1. High levels of CXCR1 and CXCR2 in bone marrow sections from <em>Gata1</em><sup>low</sup> mice. A</strong>) Representative sections from the bone marrow of wild-type and <em>Gata1</em><sup>low</sup> littermates immunostained with antibodies per CXCR1 and CXCR2. Magnification 40x. <strong>B</strong>) Computer assisted quantification of the content of the CXCR1 and CXCR2 in 5 randomly selected areas per femur from three-four mice per experimental group. Statistical analysis was done by t-test and statistically significant p values among groups are indicated within the panels. Similar results were reported in Dunbar et al[11].</p> <p><strong>Figure S8</strong>. <strong>(A) Median optical slice of a confocal stack microscopy obtained with a 63x objective.</strong> The blue arrow indicates a GFP signal present inside nucleus (shown as tridimensional image in movie 1), whereas the red arrow indicates a cell were the GFP signal is localized in the cytoplasm (shown as tridimensional image in movie 2). DAPI and GFP signals are shown separately and combined. <strong>B)</strong> <strong>Hematoxylin-eosin staining (left) and fluorescent microscopy (right) of two representative sections from the bone marrow of one </strong><strong><em>huCD34-GFPH2B</em></strong><strong> mouse. </strong>The GFP staining labels either the nuclear areas of cells with small size (1, 2 and 3) or, very rarely, the cytoplasm of large cells (4), possibly macrophages. Slides were counter stained with DAPI. Magnification 40x.</p>
The ARRIVE Essential 10: author checklist – Gastroprotective effect of Zinnia elegans extracts against ethanol-Induced induced gastric mucosal damage through downregulation of TLR4 and inflammatory cytokines.
<p>The ARRIVE Essential 10: author checklist – Gastroprotective effect of Zinnia elegans extracts against ethanol-Induced induced gastric mucosal damage through downregulation of TLR4 and inflammatory cytokines.</p>
Biohybrid microrobots regulate colonic cytokine and epithelium barrier in inflammatory bowel disease
<p>Cytokines have been identified as key contributors to the development of inflammatory bowel disease (IBD), yet conventional treatments often prove inadequate and carry substantial side effects. Here, we show an innovative biohybrid robotic system, termed 'algae-MΦNP-robot', for addressing IBD by actively neutralizing colonic cytokine levels. Our approach combines moving green microalgae with macrophage membrane-coated nanoparticles (MΦNPs) to efficiently capture pro-inflammatory cytokines 'on-the-fly'. The dynamic algae-MΦNP-robots outperform static counterparts by enhancing cytokine removal through continuous movement, better distribution, and extended retention in the colon. This system is encapsulated within an oral capsule, which shields it from gastric acidity and ensures functionality upon reaching the targeted disease site. The resulting algae-MΦNP-robot capsule effectively regulates cytokine levels, facilitating the healing of damaged epithelial barriers. It shows markedly improved prevention and treatment efficacy in a mouse model of IBD and demonstrates an excellent biosafety profile. Overall, our biohybrid algae-MΦNP-robot system offers a promising and efficient solution for IBD, addressing cytokine-related inflammation effectively.</p>
Colonic cytokines and chemokines in DNBS colitis
<p>Abdominal pain in irritable bowel syndrome and inflammatory bowel disease is thought to be driven by processes that sensitize sensory nerves innervating the gut. How sensory nerves become sensitized is not clear, but their terminals in the gut are surrounded by enteric glia. Here, we tested the hypothesis that intercellular enteric glia-to-nociceptor signaling contributes to visceral hypersensitivity during inflammation. In vivo and in vitro models of acute inflammation were used in combination with protein and RNA labeling, and cellular assays of activity and mediator release. Mechanisms of interaction between glia and nociceptors were studied using <em><span>Trpv1</span></em><em><sup>Cre;GCaMP5gtdT</sup><span>;GFAP-hM3Dq </span></em>mice, in which glial activity is controlled by chemogenetics while simultaneously recording nociceptor activity using calcium imaging. Mice lacking glial connexin-43 were used in combination with visceromotor reflex recordings to disrupt glial intercellular signaling and study its impact on visceral sensitivity. Acute colitis induces a transient increase in proinflammatory cytokines including IL-1β, which is produced in part by glia and facilitates glial connexin-43 function. Provoking glial activity under these conditions changes the normal benign influence of glia on nociceptors to one where glia have a sensitizing effect on gut-innervating nociceptors. The mechanisms responsible for glial-driven visceral hypersensitivity involve an upregulation of glial COX-2 and an increase in stimulated glial PGE2 release which acts on nociceptor EP4 receptors. In vivo recordings show that colonic IL-1β shifts normal innocuous stimuli toward a noxious range through mechanisms that require glial connexin-43. Enteric glia sensitize gut nociceptors during inflammation. Cell-specific therapies targeting the glial mechanisms identified here could benefit treatments for visceral pain.</p>
Data for Characterization of cytokine response to intraperitoneally administered LPS & subdiaphragmatic branch vagus nerve stimulation in rat model
<p>These are the data files used for publication "Characterization of cytokine response to intraperitoneally administered LPS & subdiaphragmatic branch vagus nerve stimulation in rat model" to be published in PLOS ONE.</p>
Cytokines in malaria patient
<p>this demographic data and result of cytokines to malaria patient in East Nile locality, Khartoum Sudan</p>
Elimination of HSV-2 infected cells is mediated predominantly by paracrine effects of tissue-resident T cell derived cytokines
<p>Movies associated with manuscript entitled "Elimination of HSV-2 infected cells is mediated predominantly by paracrine effects of tissue-resident T cell derived cytokines"</p> <p>available on https://doi.org/10.1101/610634 </p>
Multi-omic Mapping of Human Pancreatic Islet Endoplasmic Reticulum and Cytokine Stress Responses Provide Type 2 Diabetes Genetic Insights
<p>The following data accompanying the manuscript can be found here:</p> <ul> <li>Expression (bulk RNA-seq & scRNA-seq) matrices</li> <li>Chromatin accessibility (bulk ATAC-seq) matrices</li> <li>TDF files for IGV browser visualization of cis-regulatory elements</li> </ul>
Anti-cytokine storm activity of fraxin and quercetin, alone and in combination, and their possible molecular mechanisms via TLR4 and PPARγ signaling pathways in LPS-induced RAW 264.7 cell line article data
<p>Anti-cytokine storm activity of fraxin and quercetin, alone and in combination, and their possible molecular mechanisms via TLR4 and PPARγ signaling pathways in LPS-induced RAW 264.7 cell line article data</p>
Anti-cytokine storm activity of fraxin and quercetin, alone and in combination, and their possible molecular mechanisms via TLR4 and PPARγ signaling pathways in LPS-induced RAW 264.7 cell line article data
<p>Anti-cytokine storm activity of fraxin and quercetin, alone and in combination, and their possible molecular mechanisms via TLR4 and PPARγ signaling pathways in LPS-induced RAW 264.7 cell line article data</p>
Fig. 8. Ochrathinols A in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 8. Ochrathinols A (±)-1 compensated the NAD+/NADH ratio induced by LPS. Cells were exposed to 0.1 μg/mL LPS and co-treated with compounds of (±)-1 (10 μM) for 24 h. Intracellular NAD+/NADH ratios were determined by NAD+/NADH assay kit. Data are shown as mean ± SD (n = 3). *P <0.05, ****P <0.001 vs. LPS group, n = 3. P value was assessed by two-tailed Student's t-test.
Fig. 7 in Ochrathinols A and B, two pairs of sulfur-containing racemates from an Antarctic fungus Aspergillus ochraceopetaliformis SCSIO 05702 inhibit LPS-induced pro-inflammatory cytokines and NO production
Fig. 7. Anti-inflammation activity of ochrathinols A and B ((±)-1, (±)-2). Cells were exposed to 0.1 μg/mL LPS and co-treated with compounds of (+)-1, ()-1, (±)-1, (+)-2, ()-2, (±)-2 (10 μM) for 24 h, respectively. (A) (±)-1 reduced the release of LPS-induced IL-6, TNF-α, and MCP-1 in culture medium, n = 3. (B) qPCR analysis of pro-inflammatory cytokines genes (IL-1β, IL-6, TNF-α, and MCP-1) normalized by β-actin, n = 3. All data are presented as the mean ± SD of three independent experiments. ns, P> 0.05, *P <0.05, **P <0.01, ***P <0.005, ****P <0.001 vs. LPS group; #P <0.05, ##P <0.01, ###P <0.005, ####P <0.001 vs. control group, n = 3. P value was assessed by two-tailed Student's t-test.
Secondary Analysis of Gut Hormones and Inflammatory Cytokines in Fasting Subjects
ClinicalTrials.gov study NCT01257841. IPD Sharing: Not stated. Countries: 1. Publications: 3.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.