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opencc-zeroDec 2017View details →

Data from: Microglia responses to pro-inflammatory stimuli (LPS, IFNγ+TNFα) and reprogramming by resolving cytokines (IL-4, IL-10)

Microglia respond to CNS injuries and diseases with complex reactions, often called "activation." A pro-inflammatory phenotype (also called classical or M1 activation) lies at one extreme of the reactivity spectrum. There were several motivations for this study. First, bacterial endotoxin (lipopolysaccharide, LPS) is the most commonly used pro-inflammatory stimulus for microglia, both in vitro and in vivo; however, pro-inflammatory cytokines (e.g., IFNγ, TNFα) rather than LPS will be encountered with sterile CNS damage and disease. We lack direct comparisons of responses between LPS and such cytokines. Second, while transcriptional profiling is providing substantial data on microglial responses to LPS, these studies mainly use mouse cells and models, and there is increasing evidence that responses of rat microglia can differ. Third, the cytokine milieu is dynamic after acute CNS damage, and an important question in microglial biology is: How malleable are their responses? There are very few studies of effects of resolving cytokines, particularly for rat microglia, and much of the work has focused on pro-inflammatory outcomes. Here, we first exposed primary rat microglia to LPS or to IFNγ+TNFα (I+T) and compared hallmark functional (nitric oxide production, migration) and molecular responses (almost 100 genes), including surface receptors that can be considered part of the sensome. Protein changes for exemplary molecules were also quantified: ARG1, CD206/MRC1, COX-2, iNOS, and PYK2. Despite some similarities, there were notable differences in responses to LPS and I+T. For instance, LPS often evoked higher pro-inflammatory gene expression and also increased several anti-inflammatory genes. Second, we compared the ability of two anti-inflammatory, resolving cytokines (IL-4, IL-10), to counteract responses to LPS and I+T. IL-4 was more effective after I+T than after LPS, and IL-10 was surprisingly ineffective after either stimulus. These results should prove useful in modeling microglial reactivity in vitro; and comparing transcriptional responses to sterile CNS inflammation in vivo.

opencc-zeroMay 2019View details →

Data from: Genetic ancestry and population differences in levels of inflammatory cytokines in women: role for evolutionary selection and environmental factors

Background: Selection pressure due to exposure to infectious pathogens endemic to Africa may explain distinct genetic variations in immune response genes. However, the impact of those genetic variations on human immunity remains understudied, especially within the context of modern lifestyles and living environments, which are drastically different from early humans in sub Saharan Africa. There are few data on population differences in constitutional immune environment, where genetic ancestry and environment are likely two primary sources of variation. Methods and Findings: In a study integrating genetic, molecular and epidemiological data, we examined population differences in plasma levels of 14 cytokines involved in innate and adaptive immunity, including those implicated in chronic inflammation, and possible contributing factors to such differences, in 914 AA and 855 EA women. We observed significant differences in 7 cytokines, including higher plasma levels of CCL2, CCL11, IL4 and IL10 in EAs and higher levels of IL1RA and IFNα2 in AAs. Analyses of a wide range of demographic and lifestyle factors showed significant impact, with age, education level, obesity, smoking, and alcohol intake, accounting for some, but not all, observed population differences for the cytokines examined. Levels of two pro-inflammatory chemokines, CCL2 and CCL11, were strongly associated with percent of African ancestry among AAs. The signal was pinpointed through admixture mapping to local ancestry at 1q23, with fine-mapping analysis refined to the Duffy-null allele of rs2814778. In AA women, this variant was a major determinant of systemic levels of CCL2 (p=1.1e-58) and CCL11 (p=2.2e-110), accounting for 19% and 40% of the phenotypic variance, respectively. Conclusion: Our data reveal strong ancestral footprints in inflammatory chemokine regulation. The Duffy-null allele may indicate a loss of the buffering function for chemokine levels. The substantial immune differences by ancestry may have broad implications to health disparities between AA and EA populations.

opencc-zeroJan 2022View details →

Inflammatory cytokines and risk of gestational diabetes

Background: Over the last decade, an emerging role of novel cytokines in the pathogenesis of gestational diabetes mellitus (GDM) has been proposed by researches. The present study was performed to provide a more accurate estimate of the effect size of the association between leptin, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) and risk of GDM. Methods: Online databases were looked up to August 2021 using the search string: (leptin OR TNF-α OR IL-6) AND "gestational diabetes". Observational studies investigating the association of the selected cytokines and risk of GDM were included. Odds ratios and their 95% confidence intervals (CIs) were used to estimate pooled effect. Results: 19 studies were included in the meta-analysis (6792 women; 1405 diagnosed with GDM). A significant association was found between higher circulating leptin and risk of GDM and the pooled estimate was 1.15 (95%CI: 1.05, 1.26). Higher circulating levels of IL-6 and TNF-α were associated with increased risk of GDM and the pooled estimates were 2.00 (95%CI: 1.20, 3.31) and 1.29 (95%CI: 1.13, 1.46), respectively. Conclusions: The selected cytokines might be used as potential markers in predicting GDM and considered as contributing factors to the GDM pathogenesis.

Fig. 6 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. 6. Chiral HPLC analyses of ochrathinol B (±)-2.

Fig. 4 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. 4. Experimental and calculated ECD spectra of (±)-1, (±)-2, and 4.

Fig. 3. X 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. 3. X-ray crystallographic structures of compounds 1–3.

Fig. 2 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. 2. Key COSY (bold) and HMBC (arrows) correlations of 1 4.

Fig. 5 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. 5. Chiral HPLC analyses of ochrathinol A (±)-1.

Fig. 1 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. 1. Structures of compounds 1–4.

closedIPD-NOFeb 2026View details →

Risk Factor Analysis for Charcot Foot in Patients With Diabetes Mellitus: The Interplay of Inflammatory Cytokines and Metabolic Factors

ClinicalTrials.gov study NCT07139184. IPD Sharing: NO. Countries: 0. Publications: 10.

closedIPD-NOFeb 2026View details →

Pancreatitis CytoSorbents (CytoSorb®) Inflammatory Cytokine Removal

ClinicalTrials.gov study NCT03082469. IPD Sharing: NO. Countries: 0. Publications: 1.

restrictedIPD-UNDECIDEDFeb 2026View details →

Inflammatory Cytokine Quantification in Infants

ClinicalTrials.gov study NCT01155830. IPD Sharing: Not stated. Countries: 1. Publications: 0.

closedIPD-NOFeb 2026View details →

Effects of Radiofrequency Ablation of Posterior Nasal Nerves on Inflammatory Cytokines, Peak Nasal Inspiratory Flow, and Nasal Blood Flow in Patients With Chronic Rhinitis

ClinicalTrials.gov study NCT05648565. IPD Sharing: NO. Countries: 1. Publications: 0.

publicJan 2022View details →

Inflammatory cytokines and risk of gestational diabetes

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publicJun 2019View details →

Data from: Microglia responses to pro-inflammatory stimuli (LPS, IFNγ+TNFα) and reprogramming by resolving cytokines (IL-4, IL-10)

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