Background: Several chronic inflammatory diseases are characterized by inappropriate CD4+ T cell response. In the present study, we assessed the ability of Capparis spinosa L. (CS) preparation to orientate, in vivo, the immune response mediated by CD4+ T cells towards an anti-inflammatory response.
BackgroundCapparis Spinosa L. is an aromatic plant growing wild in dry regions around the Mediterranean basin. Capparis Spinosa was shown to possess several properties such as antioxidant, antifungal, and anti-hepatotoxic actions. In this work, we aimed to evaluate immunomodulatory properties of Capparis Spinosa leaf extracts in vitro on human peripheral blood mononuclear cells (PBMCs) from healthy individuals.ResultsUsing MTT assay, we identified a range of Capparis Spinosa doses, which were not toxic. Unexpectedly, we found out that Capparis Spinosa aqueous fraction exhibited an increase in cell metabolic activity, even though similar doses did not affect cell proliferation as shown by CFSE. Interestingly, Capparis Spinosa aqueous fraction appeared to induce an overall anti-inflammatory response through significant inhibition of IL-17 and induction of IL-4 gene expression when PBMCs were treated with the non toxic doses of 100 and/or 500 μg/ml. Phytoscreening analysis of the used Capparis Spinosa preparations showed that these contain tannins; sterols, alkaloids; polyphenols and flavonoids. Surprisingly, quantification assays showed that our Capparis Spinosa preparation contains low amounts of polyphenols relative to Capparis Spinosa used in other studies. This Capparis Spinosa also appeared to act as a weaker scavenging free radical agent as evidenced by DPPH radical scavenging test. Finally, polyphenolic compounds including catechin, caffeic acid, syringic acid, rutin and ferulic acid were identified by HPLC, in the Capparis spinosa preparation.ConclusionAltogether, these findings suggest that our Capparis Spinosa preparation contains interesting compounds, which could be used to suppress IL-17 and to enhance IL-4 gene expression in certain inflammatory situations. Other studies are underway in order to identify the compound(s) underlying this effect.Electronic supplementary materialThe online version of this article (doi:10.1186/s12865-016-0164-x) contains supplementary material, which is available to authorized users.
BackgroundGlioma is the most common type of primary brain tumor in adults. Patients with the most malignant form have an overall survival time of <16 months. Although considerable progress has been made in defining the adapted therapeutic strategies, measures to counteract tumor escape have not kept pace, due to the developed resistance of malignant glioma. In fact, identifying the nature and role of distinct tumor-infiltrating immune cells in glioma patients would decipher potential mechanisms behind therapy failure.MethodsWe integrated into our study glioma transcriptomic datasets from the Cancer Genome Atlas (TCGA) cohort (154 GBM and 516 LGG patients). LM22 immune signature was built using CIBERSORT. Hierarchical clustering and UMAP dimensional reduction algorithms were applied to identify clusters among glioma patients either in an unsupervised or supervised way. Furthermore, differential gene expression (DGE) has been performed to unravel the top expressed genes among the identified clusters. Besides, we used the least absolute shrinkage and selection operator (LASSO) and Cox regression algorithm to set up the most valuable prognostic factor.ResultsOur study revealed, following gene enrichment analysis, the presence of two distinct groups of patients. The first group, defined as cluster 1, was characterized by the presence of immune cells known to exert efficient antitumoral immune response and was associated with better patient survival, whereas the second group, cluster 2, which exhibited a poor survival, was enriched with cells and molecules, known to set an immunosuppressive pro-tumoral microenvironment. Interestingly, we revealed that gene expression signatures were also consistent with each immune cluster function. A strong presence of activated NK cells was revealed in cluster 1. In contrast, potent immunosuppressive components such as regulatory T cells, neutrophils, and M0/M1/M2 macrophages were detected in cluster 2, where, in addition, inhibitory immune checkpoints, such as PD-1, CTLA-4, and TIM-3, were also significantly upregulated. Finally, Cox regression analysis further corroborated that tumor-infiltrating cells from cluster 2 exerted a significant impact on patient prognosis.ConclusionOur work brings to light the tight implication of immune components on glioma patient prognosis. This would contribute to potentially developing better immune-based therapeutic approaches.
Background Coronavirus disease 2019 (COVID-19), poses a threat to the global public health. Early identification of critical cases is crucial to providing timely treatment to patients. Here, we investigated whether white immune cell levels could predict respiratory decline, complications and mortality. Methods We performed a retrospective study including 119 patients presenting with COVID-19. We divided our cohort into two categories, using two different classifications. Comparison tests, prediction analysis and the logistic regression analysis were used in this study. Results The study revealed that a rise in neutrophils levels was associated with respiratory deterioration and intubation. In contrast, neutrophils levels plateaued in patients who remained stable. Neutrophils levels, during the first 5 days of hospitalization, positively correlated with the procalcitonin and C-reactive protein levels. Interestingly, neutrophils levels at day 5 proved to be a better predictor of intubation and acute respiratory distress syndrome than initial neutrophils counts, C-reactive protein or procalcitonin. Neutrophils counts at day 5 higher than 7,7 (109/l) (normal range: 1,4–7,7 (109/L) also effectively predicted patient mortality, independently of usual clinical classifications. Moreover, binary logistic regression with stratified revealed that neutrophils at day5 > 7,7 (109/l) was an independent risk factor of mortality and acute respiratory distress syndrome. Finally, neutrophils levels at day 5 and the proinflammatory cytokine IL-6 were correlated, which suggested a mechanistic link. Conclusions Our data showed that neutrophils count at day 5, rather than at admission, proved to be an excellent predictor of complications and mortality during hospitalization and could be used to improve COVID-19 patients’management.
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