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Background. The Neutrophil-to-Lymphocyte Ratio (NLR) and the Platelet-to-Lymphocyte Ratio (PLR) are inflammatory biomarkers for several diseases, such as cancer and cardiovascular morbidities; however, there are currently few studies on kidney diseases. We aimed to evaluate nondialysis patients and determine the association of NLR and PLR with inflammation in these patients. Methods. A prospective cross-sectional study was conducted with 85 patients at different stages of chronic kidney disease (CKD), treated at the Kidney Disease Prevention Center of the University Hospital of the Federal University of Maranhão. This study included adult nondialysis patients diagnosed with CKD. The participants’ blood samples were collected for a high-sensitivity C-reactive protein (hs-CRP) test and blood count. They were divided into two groups according to the presence or absence of inflammation based on the hs-CRP value (<0.5 mg/dL). NLR and PLR were calculated based on the absolute number of neutrophils, lymphocytes, and platelets and were compared between them and with hs-CRP. Statistical analysis was performed using the Stata software, with the Shapiro–Wilk, Mann–Whitney, Spearman’s Correlation, and receiver operating characteristic curve tests. This study was approved by the local ethics committee. Results. The participants were categorized into two groups: with inflammation (n = 64) and without inflammation (n = 21). The mean age was 61.43 ± 14.63 y. The NLR and PLR values were significantly different between the groups with and without inflammation ( p = 0.045 and p = 0.004 , respectively). However, only PLR showed a significant positive correlation with hs-CRP ( p = 0.015 ). The best cutoff point for NLR to detect inflammation was 1.98, with 76.19% sensitivity and 48.44% specificity. For PLR, it was 116.07, with 85.71% sensitivity and 51.56% specificity. There was no significant difference between the area under the NLR and PLR curve (0.71 vs. 0.64; p = 0.186 ) for this population. Conclusions. This study showed that PLR was positively correlated with hs-CRP in nondialysis CKD patients and can be used to identify inflammation in this population.

ObjectivesThe purpose of this study was to evaluate the effect of gabapentin on Ehrlich tumor growth in Swiss mice, a highly aggressive and inflammatory tumor model. Mice were grouped into sets of 5 animals and treated from days 2 to 8 with gabapentin 30 mg/kg body weight (G30) or 100 mg/kg body weight (G100), or normal sterile saline (control).ResultsThe mice were euthanized on day 10. Tumor growth, tumoricidal agents and inflammatory cytokines levels were assessed. At day 10, G30 and G100 mice gained weight, but there were no differences in tumor cell count or in ascites volume. In G100, there was a reduction in arginase and an increase in SOD activities. There was an increase in IL-6 and MCP-1 levels, especially in G100, but no alterations in TNF-α. There was no direct evidence of tumor induction by gabapentin. However, the findings suggest that its use modulates immune response to a more effector and less deleterious profile, with increase in activity of anti-oxidant enzymes and in cytokines that favor activation of macrophages, which could improve the general status of the tumor host.Electronic supplementary materialThe online version of this article (10.1186/s13104-019-4103-9) contains supplementary material, which is available to authorized users.

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Dendritic cells (DCs) are the most efficient antigen-presenting cells and link the innate immune sensing of the environment to the initiation of adaptive immune responses, which may be directed to either acceptance or elimination of the recognized antigen. In cancer patients, though DCs would be expected to present tumor antigens to T lymphocytes and induce tumor-eliminating responses, this is frequently not the case. The complex tumor microenvironment subverts the immune response, blocks some effector mechanisms, and drives others to support tumor growth. Chronic inflammation in a tumor microenvironment is believed to contribute to the induction of such regulatory/tolerogenic response. Among the various mediators of the modulatory switch in chronic inflammation is the “antidanger signal” chaperone, heat shock protein 27 (Hsp27), that has been described, interestingly, to be associated with cell migration and drug resistance of breast cancer cells. Thus, here, we investigated the expression of Hsp27 during the differentiation of monocyte-derived DCs (Mo-DCs) from healthy donors and breast cancer patients and evaluated their surface phenotype, cytokine secretion pattern, and lymphostimulatory activity. Surface phenotype and lymphocyte proliferation were evaluated by flow cytometry, interferon- (IFN-) γ, and interleukin- (IL-) 10 secretion, by ELISA and Hsp27 expression, by quantitative polymerase chain reaction (qPCR). Mo-DCs from cancer patients presented decreased expression of DC maturation markers, decreased ability to induce allogeneic lymphocyte proliferation, and increased IL-10 secretion. In coculture with breast cancer cell lines, healthy donors' Mo-DCs showed phenotype changes similar to those found in patients' cells. Interestingly, patients' monocytes expressed less GM-CSF and IL-4 receptors than healthy donors' monocytes and Hsp27 expression was significantly higher in patients' Mo-DCs (and in tumor samples). Both phenomena could contribute to the phenotypic bias of breast cancer patients' Mo-DCs and might prove potential targets for the development of new immunotherapeutic approaches for breast cancer.