Renal involvement in Systemic Lupus Erythematous (SLE) patients is one of the leading causes of morbidity and a significant contributor to mortality. It’s estimated that nearly 50% of SLE individuals develop kidney disease in the first year of the diagnosis. Class IV lupus nephritis (LN-IV) is the class of lupus nephritis most common in Colombian patients with SLE. Altered miRNAs expression levels have been reported in human autoimmune diseases including lupus. Variations in the expression pattern of peripheral blood circulating miRNAs specific for this class of lupus nephritis could be correlated with the pathophysiological status of this group of individuals. The aim of this study was to evaluate the relative abundance of circulating microRNAs in peripheral blood from Colombian patients with LN-IV. Circulating miRNAs in plasma of patients with diagnosis of LN-IV were compared with individuals without renal involvement (LNN group) and healthy individuals (CTL group). Total RNA was extracted from 10 ml of venous blood and subsequently sequenced using Illumina. The sequences were processed and these were analyzed using miRBase and Ensembl databases. Differential gene expression analysis was carried out with edgeR and functional analysis were done with DIANA-miRPath. Analysis was carried out using as variables of selection fold change (≥2 o ≤-2) and false discovery rate (0.05). We identified 24 circulating microRNAs with differential abundance between LN-IV and CTL groups, fourteen of these microRNAs are described for the first time to lupus nephritis (hsa-miR-589-3p, hsa-miR-1260b, hsa-miR-4511, hsa-miR-485-5p, hsa-miR-584-5p, hsa-miR-543, hsa-miR-153-3p, hsa-miR-6087, hsa-miR-3942-5p, hsa-miR-7977, hsa-miR-323b-3p, hsa-miR-4732-3p and hsa-miR-6741-3p). These changes in the abundance of miRNAs could be interpreted as alterations in the miRNAs-mRNA regulatory network in the pathogenesis of LN, preceding the clinical onset of the disease. The findings thus contribute to understanding the disease process and are likely to pave the way towards identifying disease biomarkers for early diagnosis of LN.

Renal involvement is one of the most severe manifestations of systemic lupus erythematosus (SLE). Renal biopsy is the gold standard when it comes to knowing whether a patient has lupus nephritis, and the degree of renal disease present. However, the biopsy has various complications, bleeding being the most common. Therefore, the development of alternative, non-invasive diagnostic tests for kidney disease in patients with SLE is a priority. Micro RNAs (miRNAs) are differentially expressed in various tissues, and changes in their expression have been associated with several pathological processes. The aim of this study was to identify changes in the abundance of miRNAs in plasma samples from patients with lupus nephritis that could potentially allow the diagnosis of renal damage in SLE patients. This is an observational case-control cross-sectional study, in which we characterized the differential abundance profiles of miRNAs among patients with different degrees of lupus compared with SLE patients without renal involvement and healthy control individuals. We found 89 miRNAs with changes in their abundance between lupus nephritis patients and healthy controls, and 17 miRNAs that showed significant variations between SLE patients with or without renal involvement. Validation for qPCR of a group of miRNAs on additional samples from lupus patients with or without nephritis, and from healthy individuals, showed that five miRNAs presented an average detection sensitivity of 97%, a specificity of 70.3%, a positive predictive value of 82.5%, a negative predictive value of 96% and a diagnosis efficiency of 87.9%. These results strongly suggest that miR-221-5p, miR-380-3p, miR-556-5p, miR-758-3p and miR-3074-3p are potential diagnostic biomarkers of lupus nephritis in patients with SLE. The observed differential pattern of miRNA abundance may have functional implications in the pathophysiology of SLE renal damage.

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Helicobacter pylori (H. pylori) is classified by the World Health Organization (WHO) as a group I carcinogen and is one of the most efficient human pathogens with over half of the world's population colonized by this gram-negative spiral bacterium. H. pylori can cause a chronic infection in the stomach during early childhood that persists throughout life due to diverse mechanisms of immune response evasion. H. pylori has several factors strongly associated with increased risk of disease such as toxins, adhesins, and chemoattractants, some of which are highly polymorphic, phase variable, and have different functions. Conventional treatments involve the use of antibiotics. However, treatment frequently fails due to the resistance H. pylori has progressively developed to antibiotics. This creates the need for different treatments made possible by identifying new therapeutic targets in the pathogen’s genome.The purpose of this study was an in silico prediction of T- and B- epitopes in H. pylori proteins. Twenty-two external membrane proteins from H. pylori Strain 26695 (accession number NC_000915) were identified using the web tool Vaxign (http://www.violinet.org/vaxign/). A total of one-hundred epitopes (60 class I epitopes and 40 class II epitopes) that could be used to develop novel non-antibiotics drugs for an H. pylori infection were predicted.

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Background and aims Prolactin has been found to be associated with immune regulation in SLE. The aim of this study is to determine the correlation between high prolactin level in comparison with IL -6 with lupus nephritis disease activity in UKMMC. Methods In this cross-sectional study, the analysis was conducted in SLE patients who attended Nephrology clinic in UKMMC from August 2015 till February 2016 Results Out of 43 patients with lupus nephritis, 27.9% of the patients had raised serum prolactin. The median of serum prolactin level at 0 min was 19.91 ng/ml (IQR: 15.95-22.65 ) for active lupus nephritis that was significantly higher as compared to the median of serum prolactin level 14.34 ng/ml (IQR: 11.09-18.70 ) for patients in remission (p=0.014). The serum prolactin level was positively correlated to SLEDAI (rho s : 0.449, p=0.003 ) and UPCI level in lupus nephritis patients (rho s : 0.241, p=0.032). Assessment of serum IL-6 levels found that the active lupus nephritis patients were having a higher median level of 65.91 pg/ml (21.96-146.14) compared to in remission level of 15.84 pg/ml (IQR: 8.38-92.84), (p=0.039). ROC curve analysis of serum prolactin 0 min and serum prolactin 30 min and IL-6 level for prediction of SLE diseases activity provide the cutoff value of serum prolactin 0 min was 14.63 ng/ml with sensitivity 91.7% and specificity 58.1% and AUC of 0.74 (p=0.015). Conclusions Baseline fasting serum prolactin level was found to be a sensitive biomarker for evaluation of lupus nephritis disease activity. Background and aims Plasmacytoid dendritic cells (pDC) are potent producers of IFNa, we investigated what additional soluble factors are produced by pDCs and the effect of pDC depletion with JNJ-56022473 (JNJ-473), a novel antibody against CD123. We then investigated which of these factors are elevated in SLE patient sera to determine potential biomarkers. Methods pDCs were isolated from healthy donor (HD) PBMC (n=6) which were stimulated with CpGc (TLR9) and imiquimod (TLR7) then analysed by RNAseq. PBMC from SLE and HD were also treated with isotype or JNJ-473 before stimulation with CpGc for 24 hour. Culture supernatant, SLE (n=33) and HD sera (n=34) was analysed by bead-based multiplex assay (Myriad U.S.A).Results TLR9 and TLR7-agonism induced the regulation of thousands of genes, many of which were different IFNa-subtypes. Transcripts of many other secreted proteins such as MCP-2/CCL8, IP-10/CXCL10, ITAC/CXCL11 and MIP-3b/ CCL19 were also upregulated. Proteins of these were also found to be significantly increased in SLE sera compared to HD.Depleting pDCs with JNJ-473 in SLE and HD PBMC cultures reduced production of many CpGc-induced proteins including IFNa, MCP-2/CCL8, IP-10/CXCL10, ITAC/CXCL11 and MIP-3b/CCL19. RNAseq of SLE PBMC treated with JNJ-473 before CpGc stimulation, confirmed significantly decreased expression of MCP-2/CCL8, IP-10/CXCL10 and ITAC/CXCL11. Conclusions We found that pDC depletion with JNJ-473 was able to prevent TLR9-induced production of IFNa and various other solub...